Objective To improve the analysis method of the blood components of Yinchenhao decoction （YCHD） in vivo and explore its anti-hepatocellular carcinoma mechanism. Methods Ultra-high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry （UPLC-Q-TOF/MS） was used to collect and analyze blood samples from mice. The mice were given a single dose of YCHD with a concentration of 0.1 g/ml and a dose of 25 ml/kg, and then the samples were collected 2 h post–administration, which was to systematically study the chemical components of YCHD in vivo. Network pharmacological methods were used to screen the components and targets of YCHD, and the targets of hepatocellular carcinoma; The common targets of YCHD and hepatocellular carcinoma were identified for GO enrichment and KEGG enrichment. Molecular docking was performed on the main targets to verify the binding ability between the active ingredients and the core targets. The relative mRNA expression levels of serine/threonine-protein kinase（AKT1） and tumor protein p53（TP53） in liver tissues were analyzed via qPCR, including the following mouse groups: mice with concanavalin A（Con-A）-induced acute liver injury without preventive administration, mice with Con-A-induced acute liver injury that received 14 d preventive oral administration of YCHD, and untreated control mice. Results ①The active ingredients of YCHD in the blood were identified by retrieving the data from the in vitro component analysis. They were chrysophanol, herniarin, aloe-emodin, and monotropein. ②The mechanism of action of the blood components against hepatocellular carcinoma （HCC） was further analyzed using network pharmacological methods, and a total of 30 components of YCHD were screened for 213 targets and 215 HCC targets. ③There were 17 intersection targets between YCHD and hepatocellular carcinoma, including AKT1, TP53, receptor tyrosine-protein kinase erbB-2 （ERBB2）, myelocytomatosis oncogene （MYC）, interleukin-1β （IL-1β）, etc. The GO enrichment results indicated that these components were primarily involved in DNA replication，chromosome segregation，leukocyte mediated immunity，leukocyte cell-cell adhesion. The KEGG enrichment results demonstrated that these components were predominantly associated with diverse cancer pathways. Additionally, the results indicated involvement in the citrate cycle （TCA cycle）, pyruvate metabolism, and p53 signaling pathway, ect. ④The results of molecular docking showed that chrysophanol, herniarin, and aloe - emodin had strong binding abilities with AKT1, TP53, ERBB2, MYC, and IL-1β. ⑤The relative expression of AKT1 and TP53 mRNA was significantly higher in the modelling group than in the control group. The relative expression of AKT1 and TP53 mRNA was significantly lower in the drug administration group than in the modelling group. Conclusion There were 4 blood components in YCHD, among which chrysophanol, herniarin, and aloe-emodin may act on AKT1, TP53, ERBB2, MYC, IL-1β and then participated in the regulation of cancer signaling pathways and p53 signaling pathway to play a role in the treatment of HCC.

ObjectiveTo observe the clinical efficacy and safety of Tangning Tongluo tablets in the treatment of nonproliferative diabetic retinopathy （DR）. MethodsFourteen research centers participated in this study， which spanned a time interval from September 2021 to May 2023. A total of 240 patients with nonproliferative DR were included and randomly assigned into an observation group （120 cases） and a control group （120 cases）. The observation group was treated with Tangning Tongluo tablets， and the control group with calcium dobesilate capsules. Both groups were treated for 24 consecutive weeks. The vision， DR progression rate， retinal microhemangioma， hemorrhage area， exudation area， glycosylated hemoglobin （HbA1c） level， and TCM syndrome score were assessed before and after treatment， and the safety was observed. ResultsThe vision changed in both groups after treatment （P<0.05）， and the observation group showed higher best corrected visual acuity （BCVA） than the control group （P<0.05）. The DR progression was slow with similar rates in the two groups. The fundus hemorrhage area and exudation area did not change significantly after treatment in both groups， while the observation group outperformed the control group in reducing the fundus hemorrhage area and exudation area. There was no significant difference in the number of microhemangiomas between the two groups before treatment. After treatment， the number of microhemangiomas decreased in both the observation group （Z=-1.437， P<0.05） and the control group （Z=-2.238， P<0.05）， and it showed no significant difference between the two groups. As the treatment time prolonged， the number of microhemangiomas gradually decreased in both groups. There was no significant difference in the HbA1c level between the two groups before treatment. After treatment， the decline in the HbA1c level showed no significant difference between the two groups. The TCM syndrome score did not have a statistically significant difference between the two groups before treatment. After treatment， neither the TCM syndrome score nor the response rate had significant difference between the two groups. With the extension of the treatment time， both groups showed amelioration of TCM syndrome compared with the baseline. ConclusionTangning Tongluo tablets are safe and effective in the treatment of nonproliferative DR， being capable of improving vision and reducing hemorrhage and exudation in the fundus.

This article summarizes Professor Huang Guicheng's clinical experience in the syndrome differentiation and treatment of lumbar spinal stenosis using the theory of"diseases of tendons,bones and collaterals".It is believed that lumbar spinal stenosis be-longs to the syndrome of deficiency in the root and excess in the superficiality,and is closely related to the three zang organs of the liv-er,spleen and kidney.Deficiency of the liver and kidney leading to a lack of the source of qi and blood,insufficiency of the spleen and stomach giving rise to phlegm and blood stasis,and the invasion of wind,cold and dampness pathogens cause the disease.The key to the pathogenesis lies in the obstruction of the collaterals.Taking the principles of"nourishing the collaterals and strengthening the healthy qi,dredging the collaterals and expelling the pathogens"as the therapeutic principles,Professor Huang is proficient in using insect drugs.The medicinal power can directly reach the collaterals,so that the collaterals can be unobstructed and the qi and blood can flow smoothly,achieving the therapeutic effect of expelling the pathogens,unblocking the collaterals and restoring the healthy qi.

Objective:To develop a novel ovarian biological age prediction model based on DNA methylation for ovarian aging assessment.Methods:A prospective cohort study method was used. From March 2024 to January 2025, we collected 96 ovarian granulosa cell samples of infertility patients due to fallopian tube factors or male factors from the Reproductive Medicine Center of the Second Affiliated Hospital of Naval Medical University. Then we analyzed DNA methylation patterns across five age-associated gene regions ( ELOVL2, miR29B2C, TRIM59, KLF14 and FHL2) in a discovery cohort comprising 63 human ovarian granulosa cell samples. Targeted bisulfite sequencing was performed through PCR amplification followed by next-generation DNA sequencing. Leveraging elastic net regression analysis, we developed a predictive model incorporating 29 methylation sites that demonstrated strong age correlation. The model was subsequently validated using an independent cohort comprising 33 human ovarian granulosa cell samples. Results:The DNA methylation age prediction model based on ovarian granulosa cells showed the following results in the discovery cohort as follows: median absolute error (MAE) was 2.534 ( R=0.742, P<0.001). In the independent validation cohort, MAE was 3.019 ( R=0.729, P<0.001). Conclusion:In this study, we utilized human ovarian granulosa cells as experimental samples to develop a novel DNA methylation-based model for predicting ovarian biological age. By integrating multiple methylation sites across five age-related gene regions, this model serves as a robust indicator of ovarian aging status.

Objective:To develop a novel ovarian biological age prediction model based on DNA methylation for ovarian aging assessment.Methods:A prospective cohort study method was used. From March 2024 to January 2025, we collected 96 ovarian granulosa cell samples of infertility patients due to fallopian tube factors or male factors from the Reproductive Medicine Center of the Second Affiliated Hospital of Naval Medical University. Then we analyzed DNA methylation patterns across five age-associated gene regions ( ELOVL2, miR29B2C, TRIM59, KLF14 and FHL2) in a discovery cohort comprising 63 human ovarian granulosa cell samples. Targeted bisulfite sequencing was performed through PCR amplification followed by next-generation DNA sequencing. Leveraging elastic net regression analysis, we developed a predictive model incorporating 29 methylation sites that demonstrated strong age correlation. The model was subsequently validated using an independent cohort comprising 33 human ovarian granulosa cell samples. Results:The DNA methylation age prediction model based on ovarian granulosa cells showed the following results in the discovery cohort as follows: median absolute error (MAE) was 2.534 ( R=0.742, P<0.001). In the independent validation cohort, MAE was 3.019 ( R=0.729, P<0.001). Conclusion:In this study, we utilized human ovarian granulosa cells as experimental samples to develop a novel DNA methylation-based model for predicting ovarian biological age. By integrating multiple methylation sites across five age-related gene regions, this model serves as a robust indicator of ovarian aging status.

This article summarizes Professor Huang Guicheng's clinical experience in the syndrome differentiation and treatment of lumbar spinal stenosis using the theory of"diseases of tendons,bones and collaterals".It is believed that lumbar spinal stenosis be-longs to the syndrome of deficiency in the root and excess in the superficiality,and is closely related to the three zang organs of the liv-er,spleen and kidney.Deficiency of the liver and kidney leading to a lack of the source of qi and blood,insufficiency of the spleen and stomach giving rise to phlegm and blood stasis,and the invasion of wind,cold and dampness pathogens cause the disease.The key to the pathogenesis lies in the obstruction of the collaterals.Taking the principles of"nourishing the collaterals and strengthening the healthy qi,dredging the collaterals and expelling the pathogens"as the therapeutic principles,Professor Huang is proficient in using insect drugs.The medicinal power can directly reach the collaterals,so that the collaterals can be unobstructed and the qi and blood can flow smoothly,achieving the therapeutic effect of expelling the pathogens,unblocking the collaterals and restoring the healthy qi.

Tongue diagnosis is an important method of TCM diagnosis and treatment.Tongue is the key link of auxiliary diagnosis of tongue feature extraction and processing,and also is the bottleneck of intelligent tongue diagnosis in traditional Chinese medicine.Using image processing,artificial intelligence technology to the tongue as a quantitative and identify characteristics of traditional Chinese medicine,looking for both conforms to the original thinking of TCM,and TCM tongue diagnosis method of accurately,has become a common concern of traditional Chinese medicine and computer field.From the mobile terminal tongue as auxiliary diagnostic system of traditional Chinese medicine tongue acquisition basic attribute,tongue diagnosis and image information building,tongue like features are required for accurate extraction and so on related key technology is analyzed,and build overall architecture,so as to provide technical reference for the tongue like intelligent diagnosis,promote the development of technology of tongue diagnosis in traditional Chinese medicine modernization.

Lung cancer remains the most frequently diagnosed cancer and the leading cause of cancer-related death worldwide, with anaplastic lymphoma kinase (ALK) fusion mutations accounting for approximately 4%-9% of cases. In recent years, there are increasing clinical evidences suggesting that the combination of ALK inhibitors with surgical treatment holds significant potential for clinical application in resectable early and locally advanced non-small cell lung cancer (NSCLC) patients. This review aims to summarize the advances in neoadjuvant targeted therapy for ALK fusion positive NSCLC and discuss its advantages and challenges in clinical practice.
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Humans ; Carcinoma, Non-Small-Cell Lung/enzymology* ; Anaplastic Lymphoma Kinase/antagonists & inhibitors* ; Lung Neoplasms/enzymology* ; Neoadjuvant Therapy/methods* ; Molecular Targeted Therapy ; Protein Kinase Inhibitors/therapeutic use*

Objective:To investigate the expression pattern,clinical significance,and the regulatory role of 2',5'-oligoadenylate synthetase 1(OAS1)in the proliferation of pancreatic ductal adenocarcinoma(PDAC)cells.Methods:Public databases such as Gene Expression Omnibus(GEO)and The Cancer Genome Atlas(TCGA)were used to analyze the expression of OAS1 in pancreatic cancer tissues.Immunohistochemical staining was applied to validate the expression level of OAS1 in PDAC tissue microarrays,and the association between OAS1 expression level and the prognosis of patients was analyzed.Real-time fluorescence quantitative PCR was performed to examine the expression level of OAS1 mRNA in different PDAC cell lines.CCK-8 assay and colony formation assay was used to assess the effect of OAS1 on the proliferation of PDAC cells after OAS1 silencing in Patu-8988 and PDC0034 cells by siRNA treatment.Further,Gene Set enrichment analysis(GSEA)was performed to screen for possible molecular mechanism of the regulatory role of OAS1 in PDAC.Cell viability and cholesterol level was analyzed after treatment with mTOR signaling activator MHY1485 in OAS1-silenced Patu-8988 and PDC0034 cells in order to verify the underlying mechanism of the regulatory role of OAS1 in PDAC cell proliferation.Results:Database analysis showed significant upregulation of OAS1 expression in pancreatic cancer tissues(P<0.05).Immunohistochemical staining results from PDAC tissue microarray showed that OAS1 expression was significantly upregulated in PDAC tissues compared with the paired paracancerous tissues,and high OAS1 expression was associated with poor prognosis(P<0.05).Real-time fluorescence quantitative PCR and Western blotting analysis show that OAS1 expression was higher in PDAC cells lines compared with normal ductal cells of the pancreas.The proliferative activity of PDAC cells decreased significantly after OAS1 silencing in Patu-8988 and PDC0034 cells(P<0.001).GSEA results indicated that OAS1 may affect PDAC cell proliferation through mTOR signaling pathway and cholesterol metabolism associated pathway.The mTOR signaling pathway may be inhibited and the total cellular cholesterol decreased after OAS1 silencing.Treatment with mammalian target of rapamycin(mTOR)activator MHY1485 partially reversed the inhibitory effect of OAS1 silencing on the proliferation and cholesterol metabolism of PDAC cells.Conclusion:OAS1 expression is upregulated in PDAC tumor tissues and cells and is associated with poor prognosis.OAS1 may promote the proliferation of pancreatic cancer cells by enhancing cholesterol metabolism through activation of the mTOR signaling pathway.

Objective:To investigate the expression pattern,clinical significance,and the regulatory role of 2',5'-oligoadenylate synthetase 1(OAS1)in the proliferation of pancreatic ductal adenocarcinoma(PDAC)cells.Methods:Public databases such as Gene Expression Omnibus(GEO)and The Cancer Genome Atlas(TCGA)were used to analyze the expression of OAS1 in pancreatic cancer tissues.Immunohistochemical staining was applied to validate the expression level of OAS1 in PDAC tissue microarrays,and the association between OAS1 expression level and the prognosis of patients was analyzed.Real-time fluorescence quantitative PCR was performed to examine the expression level of OAS1 mRNA in different PDAC cell lines.CCK-8 assay and colony formation assay was used to assess the effect of OAS1 on the proliferation of PDAC cells after OAS1 silencing in Patu-8988 and PDC0034 cells by siRNA treatment.Further,Gene Set enrichment analysis(GSEA)was performed to screen for possible molecular mechanism of the regulatory role of OAS1 in PDAC.Cell viability and cholesterol level was analyzed after treatment with mTOR signaling activator MHY1485 in OAS1-silenced Patu-8988 and PDC0034 cells in order to verify the underlying mechanism of the regulatory role of OAS1 in PDAC cell proliferation.Results:Database analysis showed significant upregulation of OAS1 expression in pancreatic cancer tissues(P<0.05).Immunohistochemical staining results from PDAC tissue microarray showed that OAS1 expression was significantly upregulated in PDAC tissues compared with the paired paracancerous tissues,and high OAS1 expression was associated with poor prognosis(P<0.05).Real-time fluorescence quantitative PCR and Western blotting analysis show that OAS1 expression was higher in PDAC cells lines compared with normal ductal cells of the pancreas.The proliferative activity of PDAC cells decreased significantly after OAS1 silencing in Patu-8988 and PDC0034 cells(P<0.001).GSEA results indicated that OAS1 may affect PDAC cell proliferation through mTOR signaling pathway and cholesterol metabolism associated pathway.The mTOR signaling pathway may be inhibited and the total cellular cholesterol decreased after OAS1 silencing.Treatment with mammalian target of rapamycin(mTOR)activator MHY1485 partially reversed the inhibitory effect of OAS1 silencing on the proliferation and cholesterol metabolism of PDAC cells.Conclusion:OAS1 expression is upregulated in PDAC tumor tissues and cells and is associated with poor prognosis.OAS1 may promote the proliferation of pancreatic cancer cells by enhancing cholesterol metabolism through activation of the mTOR signaling pathway.