0.05).The relative bioavailability of domestic EPST tablets was(96.70?14.47)%.CONCLUSION: The result of the statistical analysis showed that the two formulations of EPST were bioequivalent.

OBJECTIVE:To determine the content of glycyrrhetic acid in zhenkening capsules by RP-HPLC.METHODS:The separation was performed on Hypersil C 18,the mobile phase consisted of methanol-water-glacial acetic acid(87∶13∶2.5)with flow rate at 1.0ml/min and detection wavelength at 254nm,the column temperature was set at room temperature.RE-SULTS:The calibration cure of glycyrrhetic acide was linear in the concentration range of 10～120?g/ml(r=0.9999),the average recovery was 99.68%(RSD=0.49%).CONCLUSION:This method is simple,fast,accurate,and suitable for the determination of glycyrrhetic acid in zhenkening capsules.

ObjectiveTo evaluate the assistant effct of electroacupuncture on acute incomplete spinal cord injury treated with routine therapy.Methods9 cases who accepted routine therapy, including operation and medicine, were in control group, while other 7 cases who accepted electroacupuncture other than routine therapy were in treating group.ResultsThere were 2 cases were effective, 4 cases were improved and 3 cases were not improved in control group, while 6 cases were clinical recovery, 1 case was effective in treating group.ConclusionElectroacupuncture can improve the effect of routine therapy on acute incomplete spinal cord injury.

目的观察神经外科与针刺联合治疗急性脊髓不完全损伤的疗效。方法神经外科治疗组根据指征确定是否进行手术,药物治疗均给予激素、脱水、抗去甲肾上腺素类药物、神经营养药物,高压氧。神经外科与针刺联合治疗组除上述神经外科治疗外,采用针刺治疗,针刺处方:电针刺激夹脊穴,根据不同辨证配合远端取穴。结果神经外科治疗组9例,持续治疗 3—6个月,出院后随访6个月,6例好转,肌力有所改善,最好者可达到肌力IV—IV+级,3例无效,甚至退步,瘫痪进一步加重。神经外科与针刺联合治疗组病人5例,经针刺及电针治疗10—80天时间后,4例临床治愈,1例经针刺治疗好转后,因转入骨科手术治疗腰椎压缩性骨折时脱离针刺治疗。结论神经外科与针刺联合治疗急性脊髓损伤效果好,并能抑制脊髓损伤的进一步恶化。

Objective:To screen and analyze ferroptosis-related genes (FRG) impacting the prognosis of colorectal adenocarcinoma patients based on bioinformatics.Methods:RNA sequencing data including the clinical information of 545 colorectal adenocarcinoma patients and 602 data sets were downloaded from the Cancer Genome Atlas (TCGA) database. FRG gene sets were downloaded from FerrDb database. FRG expression dataset could be obtained after taking the intersection between FRG gene sets and TCGA database gene sets. Differentially expressed FRG and prognosis-related genes between colorectal adenocarcinoma tissues and the adjacent tissues were screened by using R software, and finally FRG influencing the prognosis of colorectal adenocarcinoma were obtained. According to protein-protein interaction networks, the interaction and the expression association of proteins were analyzed. LASSO regression analysis was used to build a risk model for patients' 5-year overall survival rate. The risk value was calculated for 509 colorectal adenocarcinoma samples in the TCGA database, and then the median risk value was taken as the cut-off value. All patients were divided into the high-risk group (≥ median risk value) and the low-risk group (< median risk value), and the survival curves of the two groups were drawn. The receiver operating characteristic (ROC) curve was drawn for predicting the 5-year overall survival rate of colorectal adenocarcinoma patients in a time-dependent way in TCGA database according to the risk value of FRG prognosis model. Cox proportional risk model was used to make univariate and multivariate survival analysis in order to screen factors affecting the prognosis. The pathway enrichment analysis of prognosis-related FRG of colorectal adenocarcinoma was performed based on gene ontology (GO) database and Kyoto Encyclopedia of Genes and Genomes (KEGG) database.Results:The clinical information of 545 patients and 602 datasets were extracted from the database. A total of differential expressed 199 FRG in colorectal adenocarcinoma and 28 prognosis-related FRG were identified. After taking the intersection, 21 FRG affecting the prognosis of colorectal adenocarcinoma patients were identified. DUOX2, NOX4, NOX1, DDIT3, JDP2, ATP6V1G2, ULK1, ATG3 were probably associated with WIPI1; expressions of NOX4, NOX5, PLIN4 were positively correlated with ATP6V1G2, while the expression of ULK1 was negatively correlated with MAPK1, MYB, FANCD2, ATG3 and ATP5MC3. LASSO regression analysis showed that 15 FRG were finally screened out (ATP5MC3, NOX4, NOX5, ALOX12B, ATG3, WIPI1, MAPK1, MYB, AKR1C1, DDIT3, JDP2, ATP6V1G2, DRD4, SLC2A3, PLIN4), and the risk model was constructed by calculating the risk value, and the risk value = NOX4×0.139-ATP5M3×0.108+NOX5×1.486+ALOX12B×0.475-ATG3×0.030-WIPI1×0.170-MAPK1×0.271-MYB×0.063+AKR1C1×0.021+DDIT3×0.186+JDP2×0.292+ATP6V1G2×0.777+DRD4×0.294+SLC2A3×0.059+PLIN4×0.113. The overall survival of patients in the high-risk group was worse than that in the low-risk group ( P < 0.001). The 5-year overall survival rate was 48.2% in the high-risk group and 76.8% in the low-risk group. Multivariate survival showed that the age and risk value were independent affecting factors of the prognosis. ROC curves revealed that the risk model constructed by using prognosis-related FRG could well predict the 5-year overall survival rate of patients (the area under the curve was 0.728). The differential expressed genes of both groups may be associated with genetic pathways such as extracellular matrix composition, extracellular structure composition and focal adhesion. Conclusions:The prognostic risk model constructed by the screened FRG can better evaluate the prognosis of colorectal adenocarcinoma patients. These FRG are expected to become new candidate biomarkers related to the prognosis of colorectal adenocarcinoma.

OBJECTIVETo analyze the impact of platelet count on the prognosis of stage II-III colorectal cancer receiving adjuvant chemotherapy.

METHODSClinical and follow-up data of 286 patients with stage II-III colorectal cancer receiving adjuvant FOLFOX chemotherapy from March 2003 to October 2011 were analyzed retrospectively. Associations of baseline blood platelet count before chemotherapy and nadir blood platelet count during chemotherapy with relapse and death after adjuvant chemotherapy were analyzed by ROC curve and the optimal cutoff was selected. The association of the blood platelet count and the prognosis was analyzed by Kaplan-Meier and Cox regression model.

RESULTSROC curve showed the baseline blood platelet count was associated with recurrence (AUC=0.588, P=0.034). The optimal cutoff affecting recurrence was 276×10(9)/L. Kaplan-Meier showed those with baseline platelet count >276×10(9)/L receiving adjuvant chemotherapy had worse disease free survival (DFS) than those with baseline platelet count ≤276×10(9)/L, whose 5-year disease free survival(DFS) was 66% and 80% respectively (P=0.013). Cox regression analysis revealed baseline platelet count >276×10(9)/L was an independent unfavorable factor for DFS of adjuvant chemotherapy in colorectal cancer (HR=1.865, 95% CI: 1.108-3.141, P=0.019).

CONCLUSIONColorectal cancer patients receiving adjuvant chemotherapy with baseline platelet count >276×10(9)/L have worse prognosis.

Antineoplastic Combined Chemotherapy Protocols ; Chemotherapy, Adjuvant ; Colonic Neoplasms ; Colorectal Neoplasms ; Disease-Free Survival ; Fluorouracil ; Humans ; Leucovorin ; Neoplasm Staging ; Organoplatinum Compounds ; Platelet Count ; Prognosis ; Recurrence ; Retrospective Studies

Objective:To study the application effect of modified butterfly needle fixation method for implantable venous access port in breast cancer patients, in order to povide reference for the clinical applicaiton.Methods:A total of 300 patients with breast cancer from Janurary to December 2019 in Sun Yat-Sen University Cancer Center were divided into two groups by random digits table method: experimental group and control group, 150 cases in each group. The experimental group was treated with modified implantable intravenous port butterfly needle fixation method, while the control group was treated with conventional fixation method. The Visual Analogue Scale of pain during needle extraction, the incidence of needle stick injury and the time of needle extraction were measured between the two groups.Results:The Visual Analogue Scale of pain, the time of needle pulling were (4.01±0.89) points, (2.71±0.52) min in the control group, and (1.84±0.84) points, (1.86±0.39) min in the experimental group, the differences were statistically significant ( t values were -21.70, -16.02, P<0.01). The incidence of needle stick injury was 4.00% (6/150) in the control group and no needlestick injury event occurred in the experimental group, the difference was statistically significant (Fisher exact probability, P<0.05). Conclusions:The modified method of dressing fixation can effectively reduce the pain during needle pulling, reduce the incidence of needle stick injury, and effectively shorten the time of needle pulling.

This article provides an interpretive review of the "2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation", which was updated and published by the American College of Cardiology (ACC), the American Heart Association (AHA), the American College of Chest Physicians (ACCP), and the Heart Rhythm Society (HRS) based on the latest clinical evidence. It delves into the classification and management strategies for atrial fibrillation (AF), grounded in the most current evidence-based medical research. The guideline offers significant updates in various aspects such as the definition and staging of AF, clinical evaluation and treatment, modification of risk factors, prevention of thromboembolism, and management of specific populations. Notably, the introduction of a new staging model for AF and corresponding management strategies stands out, underscoring the importance of prevention and early intervention. This article focuses on the three pillars of integrated AF management—stroke risk assessment, modification of risk factors, and management of specific patient groups, in addition to rate and rhythm control, analyzes their substantial significance in clinical practice and guides clinicians in providing more precise treatment.

ObjectiveTo investigate the effect of Stemona tuberosa alkaloids （STA） on apoptosis and phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） and c-Jun N-terminal kinase/p38 mitogen-activated protein kinase （JNK/p38 MAPK） signaling pathways in human lung cancer A549 cells. MethodA549 cells were classified into blank group and STA groups （100， 150， 200， 250， 300 mg⋅L^-1）. Thiazole blue （MTT） assay and colony formation assay were used to evaluate the proliferation of A549 cells. Apoptosis was observed based on Hoechst 33258 staining， flow cytometry， and Annexin V-FITC/PI staining. Western blot was employed to detect the expression of apoptosis-related proteins cysteine-aspartic acid protease-3 （Caspase-3）， B-cell lymphoma-2 （Bcl-2）-associated X protein （Bax）， and Bcl-2， and the expression of PI3K， phosphorylated （p）-PI3K， Akt， p-Akt， JNK， p-JNK， p38 MAPK， and p-p38 MAPK. ResultCompared with the blank group， STA groups （150， 200， 250， 300 mg⋅L^-1） demonstrated the increase in inhibition rate of cell proliferation （P<0.01） and cell clone inhibition rate， and decrease in cell clone formation rate （P<0.01）. In comparison with the blank group， STA groups showed typical characteristics of apoptosis， such as chromatin condensation and enhanced fluorescence reaction. The apoptosis rate of STA groups was significantly higher than that of the blank group （P<0.01）. Compared with the blank group， STA （150， 200， 250， 300 mg⋅L^-1） significantly up-regulated the protein expression of Caspase-3 and Bax （P<0.05， P<0.01） and down-regulated the expression of Bcl-2 protein （P<0.01）. Compared with the blank group， STA had no significant influence on the total protein expression of PI3K， Akt， JNK， and p38 MAPK. However， STA （150， 200， 250， 300 mg⋅L^-1） significantly decreased the levels of p-PI3K and p-Akt （P<0.05， P<0.01） and increased the level of p-p38 MAPK （P<0.05， P<0.01）. Compared with the blank group， STA （200， 250， 300 mg⋅L^-1） significantly raised the level of p-JNK （P<0.05， P<0.01）. ConclusionSTA can inhibit the proliferation and induce the apoptosis of A549 cells by inhibiting PI3K/Akt signaling pathway and activating JNK/p38 MAPK signaling pathway.