ObjectiveTo explore the interaction and competitive binding of Homo sapiens long intergenic non-protein-coding RNA 1134 （LINC01134） to CCCTC-binding factor CTCF， affecting the transcription of cyclin-dependent kinase inhibitor （p21） and influencing the proliferation of A549 cells， in order to investigate the possible mechanism of Astragali Radix and Hedyotis diffusa （A-H） in inhibiting A549 proliferation by regulating this axis. MethodsRNA-binding protein immunoprecipitation （RIP） assays were conducted to examine the interaction between LINC01134 and CTCF， and chromatin immunoprecipitation （ChIP） assays were used to study the effect of LINC01134 overexpression on the interaction between CTCF and p21. Stable A549 cell lines （oe-NC and oe-LINC01134） were established using lentiviral transfection， and each group was treated with 10% A-H drug-containing serum. Real-time PCR and Western blot analyses were performed to detect the effects of A-H on the expression of LINC01134， CTCF， and p21 in A549 cells. Cell counting kit-8 （CCK-8） and colony formation assays were used to assess the effects of A-H on A549 cell proliferation via LINC01134. Flow cytometry was employed to evaluate the effects of A-H on the A549 cell cycle through LINC01134， and Western blot was used to detect changes in cell cycle proteins. ResultsCompared with the IgG group， the oe-CTCF group showed a significantly increased abundance of LINC01134 aggregates （P0.01）. Compared with the oe-Vector group， p21 abundance in CTCF complexes was significantly reduced in the oe-LINC01134 group （P0.01）. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of LINC01134 and p21 （P0.05）， but had no significant regulatory effect on CTCF. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed cell viability at 72 h （P0.05）， inhibited malignant proliferation （P0.05）， and reversed the proportions of cells in the G₀/G₁ and S phases （P0.01）. Furthermore， compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of Cyclin D₁， CDK4， Cyclin E， CDK2， phosphorylated retinoblastoma protein （p-Rb）， and E2F transcription factor 3 （E2F3） （P0.01）. ConclusionA-H regulates the LINC01134-CTCF-p21 axis to block the G₁/S phase transition of A549 cell cycle， accelerate cellular senescence， and inhibit malignant proliferation.

According to the Qi-blood-body fluid theory and the association between the spleen in visceral manifestation theory of traditional Chinese medicine （TCM） and mitochondria in modern cellular biology， it is proposed that the role of the spleen in generating and transforming Qi and blood is analogous to the energy-producing function of mitochondria—both serving as fundamental power sources for vital activities of the human body. The spleen governs transportation and transformation， playing a critical role in energy metabolism and the digestion and absorption of nutrients. Similarly， mitochondria are vital for maintaining physiological functions such as cellular energy supply， cell survival， and overall human metabolism. Furthermore， spleen deficiency is closely linked to mitochondrial dysfunction. Accordingly， mitochondrial energy conversion and substance metabolism are regarded as the microscopic essence of the spleen's function in transportation and transformation. Spleen deficiency and mitochondrial dysfunction contribute to the formation of pathological products such as phlegm-turbidity and blood stasis. This aligns with the pathogenesis of chronic obstructive pulmonary disease （COPD）， with Qi deficiency as the root cause and phlegm-turbidity and blood stasis as the manifestations. Therefore， the integrative treatment of COPD should follow the therapeutic principle of invigorating the spleen and reinforcing healthy Qi， while also resolving phlegm and removing blood stasis to address both root cause and manifestations. This approach can improve the mitochondrial function， regulate energy metabolism， and reduce oxidative stress levels to alleviate COPD symptoms， slow down disease progression， and improve prognosis. By integrating the holistic concept of TCM with molecular mechanisms of modern medicine， this paper explores the pathogenesis and therapeutic principles of COPD from the spleen-mitochondria correlation. It not only provides a new direction for the modern development of TCM and the integration of Chinese and Western medicine but also offers a theoretical foundation for the integrated treatment of chronic， complex age-related diseases.

ObjectiveTo explore the interaction and competitive binding of Homo sapiens long intergenic non-protein-coding RNA 1134 （LINC01134） to CCCTC-binding factor CTCF， affecting the transcription of cyclin-dependent kinase inhibitor （p21） and influencing the proliferation of A549 cells， in order to investigate the possible mechanism of Astragali Radix and Hedyotis diffusa （A-H） in inhibiting A549 proliferation by regulating this axis. MethodsRNA-binding protein immunoprecipitation （RIP） assays were conducted to examine the interaction between LINC01134 and CTCF， and chromatin immunoprecipitation （ChIP） assays were used to study the effect of LINC01134 overexpression on the interaction between CTCF and p21. Stable A549 cell lines （oe-NC and oe-LINC01134） were established using lentiviral transfection， and each group was treated with 10% A-H drug-containing serum. Real-time PCR and Western blot analyses were performed to detect the effects of A-H on the expression of LINC01134， CTCF， and p21 in A549 cells. Cell counting kit-8 （CCK-8） and colony formation assays were used to assess the effects of A-H on A549 cell proliferation via LINC01134. Flow cytometry was employed to evaluate the effects of A-H on the A549 cell cycle through LINC01134， and Western blot was used to detect changes in cell cycle proteins. ResultsCompared with the IgG group， the oe-CTCF group showed a significantly increased abundance of LINC01134 aggregates （P0.01）. Compared with the oe-Vector group， p21 abundance in CTCF complexes was significantly reduced in the oe-LINC01134 group （P0.01）. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of LINC01134 and p21 （P0.05）， but had no significant regulatory effect on CTCF. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed cell viability at 72 h （P0.05）， inhibited malignant proliferation （P0.05）， and reversed the proportions of cells in the G₀/G₁ and S phases （P0.01）. Furthermore， compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of Cyclin D₁， CDK4， Cyclin E， CDK2， phosphorylated retinoblastoma protein （p-Rb）， and E2F transcription factor 3 （E2F3） （P0.01）. ConclusionA-H regulates the LINC01134-CTCF-p21 axis to block the G₁/S phase transition of A549 cell cycle， accelerate cellular senescence， and inhibit malignant proliferation.

According to the Qi-blood-body fluid theory and the association between the spleen in visceral manifestation theory of traditional Chinese medicine （TCM） and mitochondria in modern cellular biology， it is proposed that the role of the spleen in generating and transforming Qi and blood is analogous to the energy-producing function of mitochondria—both serving as fundamental power sources for vital activities of the human body. The spleen governs transportation and transformation， playing a critical role in energy metabolism and the digestion and absorption of nutrients. Similarly， mitochondria are vital for maintaining physiological functions such as cellular energy supply， cell survival， and overall human metabolism. Furthermore， spleen deficiency is closely linked to mitochondrial dysfunction. Accordingly， mitochondrial energy conversion and substance metabolism are regarded as the microscopic essence of the spleen's function in transportation and transformation. Spleen deficiency and mitochondrial dysfunction contribute to the formation of pathological products such as phlegm-turbidity and blood stasis. This aligns with the pathogenesis of chronic obstructive pulmonary disease （COPD）， with Qi deficiency as the root cause and phlegm-turbidity and blood stasis as the manifestations. Therefore， the integrative treatment of COPD should follow the therapeutic principle of invigorating the spleen and reinforcing healthy Qi， while also resolving phlegm and removing blood stasis to address both root cause and manifestations. This approach can improve the mitochondrial function， regulate energy metabolism， and reduce oxidative stress levels to alleviate COPD symptoms， slow down disease progression， and improve prognosis. By integrating the holistic concept of TCM with molecular mechanisms of modern medicine， this paper explores the pathogenesis and therapeutic principles of COPD from the spleen-mitochondria correlation. It not only provides a new direction for the modern development of TCM and the integration of Chinese and Western medicine but also offers a theoretical foundation for the integrated treatment of chronic， complex age-related diseases.

Myosteatosis is one of the common complications in patients with end-stage liver disease, which is significantly associated with poor outcomes after liver transplantation. Currently, diagnostic criteria of myosteatosis have not been established, and CT is the most commonly used for diagnosis. The pathogenesis of myosteatosis is multifactorial, and the pathophysiological mechanisms linking it to end-stage liver disease are not fully understood. An increasing number of scholars have recognized that the severity of myosteatosis is closely related to its clinical consequences, but there are no effective treatment options available. This article reviews the pathophysiological mechanisms and diagnostic methods of myosteatosis, and its impact on the prognosis of liver transplant recipients, and discusses current treatment strategies to provide references for the perioperative management of liver transplant recipients.

To explore the advantages of traditional Chinese medicine （TCM） and integrative TCM-Western medicine approaches in the treatment of diabetic microvascular complications （DMC）， refine key pathophysiological insights and treatment principles， and promote academic innovation and strategic research planning in the prevention and treatment of DMC. The 38th session of the Expert Salon on Diseases Responding Specifically to Traditional Chinese Medicine， hosted by the China Association of Chinese Medicine， was held in Beijing， 2024. Experts in TCM， Western medicine， and interdisciplinary fields convened to conduct a systematic discussion on the pathogenesis， diagnostic and treatment challenges， and mechanism research related to DMC， ultimately forming a consensus on key directions. Four major research recommendations were proposed. The first is addressing clinical bottlenecks in the prevention and control of DMC by optimizing TCM-based evidence evaluation systems. The second is refining TCM core pathogenesis across DMC stages and establishing corresponding "disease-pattern-time" framework. The third is innovating mechanism research strategies to facilitate a shift from holistic regulation to targeted intervention in TCM. The fourth is advancing interdisciplinary collaboration to enhance the role of TCM in new drug development， research prioritization， and guideline formulation. TCM and integrative approaches offer distinct advantages in managing DMC. With a focus on the diseases responding specifically to TCM， strengthening evidence-based support and mechanism interpretation and promoting the integration of clinical care and research innovation will provide strong momentum for the modernization of TCM and the advancement of national health strategies.

Objective To explore the relationship between PANoptosis and hepatic ischemia-reperfusion injury (HIRI), and to screen the key genes of PANoptosis in HIRI. Methods PANoptosis-related differentially expressed genes (PDG) were obtained through the Gene Expression Omnibus database and GeneCards database. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were used to explore the biological pathways related to PDG. A protein-protein interaction network was constructed. Key genes were selected, and their diagnostic value was assessed and validated in the HIRI mice. Immune cell infiltration analysis was performed based on the cell-type identification by estimating relative subsets of RNA transcripts. Results A total of 16 PDG were identified. GO analysis showed that PDG were closely related to cellular metabolism. KEGG analysis indicated that PDG were mainly enriched in cellular death pathways such as apoptosis and immune-related signaling pathways such as the tumor necrosis factor signaling pathway. GSEA results showed that key genes were mainly enriched in immune-related signaling pathways such as the mitogen-activated protein kinase (MAPK) signaling pathway. Two key genes, DFFB and TNFSF10, were identified with high accuracy in diagnosing HIRI, with areas under the curve of 0.964 and 1.000, respectively. Immune infiltration analysis showed that the control group had more infiltration of resting natural killer cells, M2 macrophages, etc., while the HIRI group had more infiltration of M0 macrophages, neutrophils, and naive B cells. Real-time quantitative polymerase chain reaction results showed that compared with the Sham group, the relative expression of DFFB messenger RNA in liver tissue of HIRI group mice increased, and the relative expression of TNFSF10 messenger RNA decreased. Cibersort analysis showed that the infiltration abundance of naive B cells was positively correlated with DFFB expression (r=0.70, P=0.035), and the infiltration abundance of M2 macrophages was positively correlated with TNFSF10 expression (r=0.68, P=0.045). Conclusions PANoptosis-related genes DFFB and TNFSF10 may be potential biomarkers and therapeutic targets for HIRI.

The global distribution of medical resources is uneven and organ shortages are becoming increasingly serious. ASEAN countries have been working hard to explore and promote local organ transplantation in order to alleviate the serious imbalance between organ donation and organ transplantation needs. However, the development of cadaveric organ donation varies among ASEAN countries, and the cadaveric organ donation rate in most countries is generally low. Since 1991, China and ASEAN have evolved from dialogue to strategic cooperation, then to a community with a shared future, and further to a comprehensive strategic partnership, all demonstrating broad prospects for cooperation. This article analyzes the current situation and challenges of organ donation and transplantation in ASEAN countries, combining field visits and its own experience, and proposes strategies for strengthening international cooperation, optimizing policy environment, enhancing technical capabilities, and increasing public awareness in the field of organ donation and transplantation under the China-ASEAN development strategy framework. The aim is to build a more equitable, efficient, and sustainable organ donation and transplantation system, contributing to the realization of global public health security and a community of common health for mankind.

Fungal keratitis represents a significant cause of blindness, with current therapeutic approaches yielding limited success. The disease's onset and progression are primarily driven by fungal virulence factors and the host's immune response. The innate immune system is the first to respond, with neutrophils playing a pivotal role in the antifungal defense. Although neutrophils are critical for pathogen clearance, their excessive or abnormal activation can lead to tissue damage, exacerbating the disease. Thus, elucidating the mechanisms underlying neutrophil activity in fungal keratitis is crucial for refining treatment strategies. This article aims to systematically review the principal antimicrobial mechanisms employed by neutrophils, including phagocytosis, degranulation, and the formation of neutrophil extracellular traps(NETs). Furthermore, it explores the crosstalk between neutrophils and macrophages, alongside their collective impact and underlying mechanisms in the context of fungal keratitis. Exploration of the mechanisms of fungal keratitis facilitates precise intervention and enhances the efficacy of treatment.

ObjectiveTo evaluate the clinical efficacy of Fuzheng Huaji Formula （扶正化积方） for chronic hepatitis B to reduce the incidence of liver cirrhosis and hepatocellular carcinoma. MethodsA retrospective cohort study was conducted， collecting medical records of 118 patients with chronic hepatitis B and 234 patients with hepatitis B-related cirrhosis who visited the hospital between January 1， 2014， and December 31， 2018. The use of Fuzheng Huaji Formula was designated as the exposure factor. Patients receiving antiviral treatment for hepatitis B without concurrent Fuzheng Huaji Formula therapy were included in the western medicine group， while those receiving antiviral treatment combined with Fuzheng Huaji Formula for a cumulative treatment lasting longer than 3 months were included in the combined treatment group. The follow-up observation period was five years. Kaplan-Meier survival analysis was used to assess the cumulative incidence of cirrhosis in patients with chronic hepatitis B and the cumulative incidence of hepatocellular carcinoma in patients with hepatitis B-related cirrhosis. Univariate and multivariate Cox regression analyses were employed to examine the factors influencing the occurrence of cirrhosis and hepatocellular carcinoma. ResultsAmong patients with chronic hepatitis B， there were 55 cases in the combined treatment group and 63 cases in the western medicine group； among patients with hepatitis B-related cirrhosis， there were 110 cases in the combined treatment group and 124 cases in the western medicine group. Five-year follow-up outcomes for chronic hepatitis B patients showed that the cumulative incidence of cirrhosis was 5.45% （3/55） in the combined treatment group and 17.46% （11/63） in the western medicine group， with a statistically significant difference between groups （Z = 2.003， P = 0.045）. Five-year follow-up outcomes for hepatitis B-related cirrhosis patients showed that the cumulative incidence of hepatocellular carcinoma was 8.18% （9/110） in the combined treatment group and 22.58% （28/124） in the western medicine group， also showing a statistically significant difference （Z = 3.007， P = 0.003）. Univariate and multivariate Cox regression analyses indicated that treatment with Fuzheng Huaji Formula is an independent protective factor in preventing the progression of chronic hepatitis B to cirrhosis and the progression of hepatitis B-related cirrhosis to hepatocellular carcinoma （P＜0.05）. ConclusionCombining Fuzheng Huaji Formula with antiviral therapy for hepatitis B can effectively intervene in the disease progression of chronic hepatitis B， reducing the incidence of cirrhosis and hepatocellular carcinoma.