The development of traditional Chinese medicine (TCM) diagnosis and treatment has undergone multiple paradigms, evolving from sporadic experiential practices to systematic approaches in syndrome differentiation and treatment and further integration of disease and syndrome frameworks. TCM is a vital component of the medical system, valued alongside Western medicine. Treatment based on syndrome differentiation embodies both personalized treatment and holistic approaches; however, the inconsistency and lack of stability in syndrome differentiation limit clinical efficacy. The existing integration of diseases and syndromes primarily relies on patchwork and embedded systems, where the full advantages of synergy between Chinese and Western medicine are not fully realized. Recently, driven by the development of diagnosis and treatment concepts and advances in analytical technology, Western medicine has been rapidly transforming from a traditional biological model to a precision medicine model. TCM faces a similar need to progress beyond traditional syndrome differentiation and disease-syndrome integration toward a more precise diagnosis and treatment paradigm. Unlike the micro-level precision trend of Western medicine, precision diagnosis and treatment in TCM is primarily reflected in data-driven applications that incorporate information at various levels, including precise syndrome differentiation, medication, disease management, and efficacy evaluation. The current priority is to accelerate the development of TCM precision diagnosis and treatment technology platforms and advance discipline construction in this area.

ObjectiveTo use bioinformatics technology to screen the molecular patterns and diagnostic biomarkers of ferroptosis closely related to psoriasis， observe the therapeutic effect of Kaixuan Jiedu core prescription on psoriasis and explore its potential mechanism through animal experiments. MethodsPsoriasis microarray data from GEO were analyzed to identify differentially expressed genes （DEGs）. Intersection with a ferroptosis gene set yielded psoriasis ferroptosis-related genes （FRGs）， which underwent correlation， consensus clustering， enrichment， and immune infiltration analyses. Core diagnostic FRGs （Hub-FRGs） were identified using random forest （RF）， support vector machine （SVM）， LASSO regression， Nomogram， and ROC analyses. In vivo， imiquimod （5% cream） induced psoriasis in mice （except controls）. Drug treatment groups received respective doses， while control and model groups received saline via daily gavage for 7 days. Back skin changes were recorded and PASI scored. Hematoxylin-eosin （HE） staining assessed histopathology. The levels of ferrous ion （Fe²⁺）， malondialdehyde （MDA）， 4-hydroxynonenal （4-HNE） and free fatty acid （FFA） in skin tissue were detected. The level of reactive oxygen species （ROS） in skin tissue was detected by immunofluorescence. Immunohistochemistry was used to detect the expression of ChaC glutathione-specific γ-glutamyl transferase 1 （CHAC1）， arachidonic acid 12-lipoxygenase β （ALOX12B）， trimotif protein 21 （TRIM21）， proliferation marker （Ki67） and nuclear transcription factor-κB （NF-κB） protein. ResultsAnalysis of GSE30999 identified 2 100 DEGs and 24 FRGs. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment revealed 1 000 biological functions and 75 pathways. After cluster analysis， combined with three machine learning algorithms， Nomogram and ROC curve analysis， the core Hub-FRGs （CHAC1， ALOX12 B， TRIM21） were obtained. Immunoinfiltration showed inactive memory CD4⁺T cells and activated dendritic cells abundance significantly correlated with Hub-FRGs. In vivo， model group vs. control showed significantly increased PASI/Baker scores （P<0.05）， epidermal hyperkeratosis， inflammatory infiltration， and elevated levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， CHAC1， ALOX12B， TRIM21， Ki67， and NF-κB （P<0.05）. Drug groups vs. model group exhibited significantly reduced scores （P<0.05）， alleviated skin lesions， and decreased levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， Hub-FRGs， Ki67， and NF-κB （P<0.05）. ConclusionKaixuan Jiedu core prescription can significantly improve the skin pathological injury of psoriasis mice， showing good therapeutic and repair effects， and its mechanism may be related to regulating the expression of ferroptosis genes CHAC1， ALOX12B and TRIM21， which are closely related to the pathogenesis of psoriasis.

ObjectiveTo use bioinformatics technology to screen the molecular patterns and diagnostic biomarkers of ferroptosis closely related to psoriasis， observe the therapeutic effect of Kaixuan Jiedu core prescription on psoriasis and explore its potential mechanism through animal experiments. MethodsPsoriasis microarray data from GEO were analyzed to identify differentially expressed genes （DEGs）. Intersection with a ferroptosis gene set yielded psoriasis ferroptosis-related genes （FRGs）， which underwent correlation， consensus clustering， enrichment， and immune infiltration analyses. Core diagnostic FRGs （Hub-FRGs） were identified using random forest （RF）， support vector machine （SVM）， LASSO regression， Nomogram， and ROC analyses. In vivo， imiquimod （5% cream） induced psoriasis in mice （except controls）. Drug treatment groups received respective doses， while control and model groups received saline via daily gavage for 7 days. Back skin changes were recorded and PASI scored. Hematoxylin-eosin （HE） staining assessed histopathology. The levels of ferrous ion （Fe²⁺）， malondialdehyde （MDA）， 4-hydroxynonenal （4-HNE） and free fatty acid （FFA） in skin tissue were detected. The level of reactive oxygen species （ROS） in skin tissue was detected by immunofluorescence. Immunohistochemistry was used to detect the expression of ChaC glutathione-specific γ-glutamyl transferase 1 （CHAC1）， arachidonic acid 12-lipoxygenase β （ALOX12B）， trimotif protein 21 （TRIM21）， proliferation marker （Ki67） and nuclear transcription factor-κB （NF-κB） protein. ResultsAnalysis of GSE30999 identified 2 100 DEGs and 24 FRGs. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment revealed 1 000 biological functions and 75 pathways. After cluster analysis， combined with three machine learning algorithms， Nomogram and ROC curve analysis， the core Hub-FRGs （CHAC1， ALOX12 B， TRIM21） were obtained. Immunoinfiltration showed inactive memory CD4⁺T cells and activated dendritic cells abundance significantly correlated with Hub-FRGs. In vivo， model group vs. control showed significantly increased PASI/Baker scores （P<0.05）， epidermal hyperkeratosis， inflammatory infiltration， and elevated levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， CHAC1， ALOX12B， TRIM21， Ki67， and NF-κB （P<0.05）. Drug groups vs. model group exhibited significantly reduced scores （P<0.05）， alleviated skin lesions， and decreased levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， Hub-FRGs， Ki67， and NF-κB （P<0.05）. ConclusionKaixuan Jiedu core prescription can significantly improve the skin pathological injury of psoriasis mice， showing good therapeutic and repair effects， and its mechanism may be related to regulating the expression of ferroptosis genes CHAC1， ALOX12B and TRIM21， which are closely related to the pathogenesis of psoriasis.

Objective: To explore the association between the Internet usage characteristics and suicidal ideation among vocational high school students, so as to provide a theoretical basis for precise intervention of suicide among vocational high school students. Methods: A total of 1 781 students were recruited from three vocational high schools in Wuhan and Xianning in March 2023 by using the cluster random sampling method. The Columbia-Suicide Severity Rating Scale and Revised Chen Internet Addiction Scale were used to measure suicidal ideation and Internet addiction, respectively. LASSO regression model was used to select influential factors related to suicidal ideation, and the gradient boosting decision tree algorithm XGBoost was used to develop prediction models and evaluate predictive performance. By calculating the SHAP values, the contribution of each influential factor was quantified. Results: The prevalence of suicidal ideation among vocational high school students was 42.22% and prevalence of Internet addiction was 26.39%. LASSO regression results indicated that age, gender, experience of being left behind, parental relationship, holding a class cadre position, using the Internet for learning, Internet use during dawn, morning and late night, Internet addiction, and depressive symptoms were all the influential factors of suicidal ideation among vocational high school students ( β= -0.05 , 0.29, 0.09, 0.27, 0.10, -0.01, 0.09, 0.05, 0.24, 0.28, 0.78, all P <0.05). The AUC of the prediction model was 0.75. The results based on SHAP values indicated that all influential factors identified through multivariate analysis contributed positively to the model predictions ( SHAP >0). Among these, depressive symptoms and parental relationship had the greatest impact on suicidal ideation ( SHAP =0.77, 0.26), and the joint effect of features with higher contribution could improve the prediction probability. Conclusions Depressive symptoms, parental relationships, Internet addiction, and time of Internet use are most important risk factors of suicidal behaviors for vocational high school students. Thus, effective interventions should be conducted to reduce their suicidal ideation.

RNA modifications constitute a crucial class of post-transcriptional chemical alterations that profoundly influence RNA stability and translational efficiency, thereby shaping cellular protein expression profiles. These diverse chemical marks are ubiquitously involved in key biological processes, including cell proliferation, differentiation, apoptosis, and metastatic potential, and they exert precise regulatory control over these functions. A major advance in the field is the recognition that RNA modifications do not act in isolation. Instead, they participate in complex, dynamic interactions—through synergistic enhancement, antagonism, competitive binding, and functional crosstalk—forming what is now termed the “RNA modification interactome” or “RNA modification interaction network.” The formation and functional operation of this interactome rely on a multilayered regulatory framework orchestrated by RNA-modifying enzymes—commonly referred to as “writers,” “erasers,” and “readers.” These enzymes exhibit hierarchical organization within signaling cascades, often functioning in upstream-downstream sequences and converging at critical regulatory nodes. Their integration is further mediated through shared regulatory elements or the assembly into multi-enzyme complexes. This intricate enzymatic network directly governs and shapes the interdependent relationships among various RNA modifications. This review systematically elucidates the molecular mechanisms underlying both direct and indirect interactions between RNA modifications. Building upon this foundation, we introduce novel quantitative assessment frameworks and predictive disease models designed to leverage these interaction patterns. Importantly, studies across multiple disease contexts have identified core downstream signaling axes driven by specific constellations of interacting RNA modifications. These findings not only deepen our understanding of how RNA modification crosstalk contributes to disease initiation and progression, but also highlight its translational potential. This potential is exemplified by the discovery of diagnostic biomarkers based on interaction signatures and the development of therapeutic strategies targeting pathogenic modification networks. Together, these insights provide a conceptual framework for understanding the dynamic and multidimensional regulatory roles of RNA modifications in cellular systems. In conclusion, the emerging concept of RNA modification crosstalk reveals the extraordinary complexity of post-transcriptional regulation and opens new research avenues. It offers critical insights into the central question of how RNA-modifying enzymes achieve substrate specificity—determining which nucleotides within specific RNA transcripts are selectively modified during defined developmental or pathological stages. Decoding these specificity determinants, shaped in large part by the modification interactome, is essential for fully understanding the biological and pathological significance of the epitranscriptome.

Objective To explore the expression level of serum long non-coding RNA(lncRNA)T342620 in patients with hepatocellular carcinoma(HCC)and the clinical value of single or combined detection with al-pha-fetoprotein(AFP)for HCC.Methods Case-control studies were conducted.A total of 69 patients with primary hepatocellular carcinoma(HCC group),32 patients with hepatitis B(hepatitis B group),20 patients with liver cirrhosis(liver cirrhosis group),30 patients after transcatheter hepatic arterial chemoembolization(TACE)for primary hepatocellular carcinoma(HCC postoperative group)and 50 healthy patients(health ex-amination group)treated in the General Hospital of Southern Theatre Command of PLA from April 2021 to May 2023 were selected as the study objects.The serum total RNA was extracted and the relative expression level of lncRNA T342620 in serum was detected by real-time quantitative PCR.Combined with the clinical di-agnosis and treatment data of patients,the correlation between its expression and pathological characteristics and serological indexes was analyzed,and the specificity and sensitivity of lncRNA T342620 alone and in com-bination with AFP in the diagnosis of HCC were analyzed by receiver operating characteristic(ROC)curve.The diagnostic efficacy was judged according to the area under the curve,and its application value in the diag-nosis of HCC was evaluated.The chi-square test was used for comparison between groups,and the Spearman method was used for correlation analysis.Results The serum expression levels of lncRNA T342620 in liver cancer group and postoperative liver cancer group were higher than those in healthy physical examination group,hepatitis B group and liver cirrhosis group,and the differences were statistically significant(P＜0.001).Clinical pathological and serological index analysis revealed that as the tumor size increased,the serum lncRNA-T342620 expression level also increased.In the HCC group,the serum lncRNA T342620 expression level was negatively correlated with albumin(ALB)and the A/G ratio(P＜0.05),while it was positively cor-related with α-L-fucosidase(AFU)and HBV-DNA(P＜0.05).In patients from the HCC postoperative group,the serum lncRNA T342620 expression level was positively correlated with total bile acid(TBA)(P＜0.05).ROC curve analysis demonstrated that when using serum lncRNA T342620 to distinguish,the sensitivi-ty and the specificity were 55.1％and 94.1％,respectively,indicating good diagnostic value.When combined with AFP detection,the sensitivity and the specificity improved to 91.3％and 91.2％,respectively,which were higher than those of individual indicators and had a superior diagnostic efficiency with area under the cuve(AUC)of 0.954 compared to AUC of AFP or lncRNA-T342620 alone(0.906,0.758),and the differ-ences were statistically significant(P＜0.05).Conclusion Serum lncRNA T342620 may be a new serological index for the auxiliary diagnosis of HCC.

Objective:To explore the expression of lncRNA ARHGAP5-AS1 in renal cancer tissues and cell lines, and the effect of ARHGAP5-AS1 on the proliferation and invasion of renal cancer cell lines and its molecular mechanism.Methods:The GEPIA database was used to analyze the expression of ARHGAP5-AS1 in renal cancer tissues, and its relationship with clinical stage, overall survival and disease-free survival of renal cancer patients was analyzed. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression level of ARHGAP5-AS1 in renal cancer cells (786-O, Caki-1, OS-RC-2, ACHN, A-498). Renal carcinoma OS-RC-2 cells were transfected with pcDNA3.1-ARHGAP5-AS1 plasmid or pcDNA3.1 plasmid, denoted as ARHGAP5-AS1 group and control group. Colony formation assay and Transwell assay were used to detect changes in the proliferation and invasion ability of OS-RC-2 cells. Dual-luciferase reporter gene experiment was used to verify the targeting relationship between ARHGAP5-AS1 and miR-155-5p. The Starbase v3.0 online database was used to analyze the correlation between the expression of ARHGAP5-AS1 and miR-155-5p in renal cancer tissues. RT-qPCR was used to detect the expression level changes of miR-155-5p. Western blotting was used to detect the expression changes of Raf/MEK/ERK molecular pathway proteins p-Raf, p-MEK, p-ERK, p-FBW7, and c-MYC. The measurement data were expressed as mean ± standard deviation ( ± s), the independent sample t-test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:ARHGAP5-AS1 was lowly expressed in renal cancer tissues ( P<0.01), and its expression level was related to the clinical stage, overall survival and disease-free survival of patients with renal cancer ( P<0.01). ARHGAP5-AS1 showed low expression in renal cancer cell lines (786-O, Caki-1, OS-RC-2, ACHN, A-498) ( P<0.01). Compared with the control group, the proliferation and invasion abilities of OS-RC-2 cells in ARHGAP5-AS1 group were significantly reduced ( P<0.01). Dual-luciferase reporter gene experiment confirmed that ARHGAP5-AS1 targets and binds to miR-155-5p ( P<0.01). The expression of ARHGAP5-AS1 and miR-155-5p in renal cancer tissues was negatively correlated ( P<0.01). Compared with the control group, the expression of miR-155-5p in OS-RC-2 cells in the ARHGAP5-AS1 group was significantly reduced ( P<0.01). Compared with the control group, the expression levels of Raf/MEK/ERK molecular pathway proteins p-Raf, p-MEK, p-ERK, p-FBW7, and c-MYC in OS-RC-2 cells in the ARHGAP5-AS1 group were reduced. Conclusions:lncRNA ARHGAP5-AS1 is lowly expressed in renal cancer tissues and is related to the clinical stage and survival of renal cancer patients. ARHGAP5-AS1 inhibits the proliferation and invasion of renal cancer cells by targeting the expression of miR-155-5p.

Fork head box O3a(FoxO3a)is a member of the O subtype family of FOX transcription factors,which plays an im-portant role as a transcriptional regulator in the occurrence and development of many diseases.Mitochondria are the major sites of cellular energy metabolism and the key organelles for cell growth and function.Mitochondrial function is regulated by man-y transcription factors.FoxO3a localizes in mitochondria and has important effects on mitochondrial function by regulating the in-teraction between the nucleus and mitochondria.Its mechanism is closely related to the regulation of mitochondrial energy metab-olism,biogenesis,autophagy,fission/fusion,and mitochondrial calcium homeostasis.This review focuses on the biological func-tions of FoxO3a and its regulation and mechanism of mitochon-drial function.

As the target of many psychoactive drugs such as hal-lucinogens,antidepressants,anxiolytics and atypical antipsychot-ics,5-HT2A receptor has been a research hotspot in the field of neuropsychopharmacology.Some key amino acid sites of 5-HT2A receptor play an important role in maintaining the specific con-formation of receptor,coupling different G proteins,and exerci-sing corresponding specific functions.Further studies have shown that mutations of these specific amino acid sites can cause changes in the affinity and potency of the corresponding ligands.Moreover,5-HT2A receptor is a typical G-protein-coupled recep-tor,and different amino acid sites in its structural domain can in-teract with different ligands,causing corresponding dynamic structural changes of the receptor,thus affecting the receptor function.Therefore,studying the relationship between the struc-ture and function of 5-HT2A receptor and key amino acid sites is of great significance for the treatment of related psychiatric dis-eases and the design of new drugs with high efficiency and low toxicity.

Hydrogen sulfide,as a third gas signal molecule and neurotransmitter,can play a neuroprotective role by anti-oxidative stress,anti-inflammatory response,metabolic inhibition and other mechanisms.It is of great significance for the occurrence and development of neurodegenerative diseases including Alzheimer's disease(AD)and Parkinson's disease(PD)mediated by neuroinflammation.This article reviews the research progress of hydrogen sulfide and neuroinflammation and its mediated neurodegenerative diseases,so as to provide new ideas for the treatment of neurodegenerative diseases.