目的 以安德森模型为基础调查湖南省社区居民口腔卫生服务利用情况,为社区口腔保健的健康宣教提供建议.方法 选取2020年7月至9月湖南省的518例社区居民作为研究对象,采用logistic回归分析年龄、文化程度、口腔保健认知、全身健康状况自我评价、健康刷牙行为和口腔卫生服务利用的关系.结果 社区居民对口腔疾病的认知情况一般,自我保健行为缺乏,卫生服务利用率较差.单因素分析结果显示,不同年龄、口腔保健认知得分、全身健康状况自我评价、健康刷牙行为的口腔就诊率比较,差异有统计学意义(P＜0.05);多因素分析结果显示,年龄 12～15 岁(β=0.834,OR=2.303,95％CI=1.327～3.998)、年龄＞30岁(β=0.939,OR=2.558,95％CI=1.573～4.158)、口腔保健认知及格(β=0.522,OR=1.686,95％CI=1.023～2.779)、全身健康状况自我评价较差(β=1.155,OR=3.174,95％CI=1.172～8.600)、健康刷牙方式良好(β=0.923,OR=2.516,95％CI=1.689～3.748)可提高口腔就诊率(P＜0.05).结论 社区居民口腔保健认知与口腔健康行为仍需加强宣传力度,建议针对家长进行社区儿童口腔保健科普,着重正确刷牙行为的宣传.

Abstract Colon carcinoma is a highly malignant tumor, its early symptoms are not obvious, and its prognosis is poor. Therefore, it is urgent to develop more prognostic markers of colon cancer. Many long non-coding RNAs (lncRNAs) have been proven to play an active role in tumor diagnosis, prognosis, and immunotherapy. On the other hand, the crucial role of immunogenic cell death (ICD) is in tumor inhibition. This paper aims to integrate ICD-related genes with lncRNAs and explore the mechanism of action of ICD-related lncRNAs in colon cancer. Therefore, this paper proposes a multi-constraint canonical correlation analysis to explore ICD-related lncRNAs. Furthermore, this paper uses univariate and Lasso-Cox regression to construct and verify the prognosis model of the top important lncRNAs. In this paper, according to the model's risk score, colon cancer samples are divided into a high-risk group and a low-risk group, and the effect of the model is verified based on the TCGA queue and GEO queue, respectively. In addition, we analyzed the similarities and differences in functional enrichment, immune infiltration, and drug sensitivity between the two risk groups in detail. There was a significant difference in the infiltrating abundance of T cells CD8 between high- and low-risk groups. Therefore, this article re-clusters T cell clusters based on single-cell sequencing (scRNA-seq) data of colon cancer. The unique pathways involved in the genes of the CD8 subpopulation of T cells and their communication with other T cell subpopulations were explored. In summary, the ICD-related lncRNAs risk model determined in this paper can provide a reference for predicting colon cancer patients' prognosis and drug sensitivity.

鼻咽癌是一种起源于鼻咽黏膜的上皮性癌,在我国主要高发于南方地区.miRNA是一类非编码的小RNA分子,在组织、血清、血浆和其他体液中稳定性表达,通过与互补的靶mRNA结合,导致mRNA翻译抑制或mRNA降解,在细胞增殖、分化过程中发挥核心作用,并在恶性肿瘤的发生、发展中发挥着促癌或抑癌作用.miRNA异常表达可通过改变癌基因和抑癌基因的表达来参与鼻咽癌的发生、转移和耐药性,在鼻咽癌的诊断和治疗中具有重要作用.研究异常表达的miRNA及其作用机制,进一步阐明鼻咽癌的发病机制,可为鼻咽癌的诊断和治疗提供新的研究方向.本文对近年来miRNA在鼻咽癌的发生、发展、诊断、治疗和预后评估中的作用进行综述,以期为miRNA调控鼻咽癌的基础研究及其转化应用提供科学依据和新思路.

Objective To investigate the effects of evodiamine on proliferation and apoptosis of 5-8F cells in nasopharyngeal carcinoma cells and the role of PI3K/AKT signaling pathway.Methods The 5-8F cells were divided into solvent control group,evodiamine (0.5,1.0,2.0,4.0μmol·L -1 ) groups and cisplatin (4.0μgmol·L -1 ) group;in addition,the 5-8F cells were divided into 5groups:solvent control group,SC79 (2.5μmol·L -1 ) group,SC79+evodiamine (2.0μmol·L -1 ) group,evodiamine (2.0μmol·L -1 ) group and LY294002 (50μmol·L -1 ) group.The cell proliferation was monitored by real time cellular analysis technology （RTCA）,the apoptosis rate was detected by annexin V-FITC/PI double fluorescence staining,and the apoptosis morphology was observed by Hoechest33342 staining.The expression levels of phosphatidylinositol 3-kinase （PI3K）,phosphorylated protein kinase B （p-AKT）,proliferating cell nuclear antigen （PCNA）,X-linked inhibitor of apoptosis （XIAP） and Survivin were detected by Western blot.Results Compared with the solvent control group,different concentrations of evodiamine (0.5,1.0,2.0,4.0μmol·L -1 ) significantly inhibited the proliferation of 5-8F cells （P＜0.05 or P＜0.01）,and the nuclear fluorescence staining and apoptosis rate of cells in evodiamine group (1.0,2.0μmol·L -1 ) increased significantly （P＜0.01）.The protein expression of PI3K,p-AKT,PCNA,XIAP and Survivin decreased significantly （P＜0.05 or P＜0.01）.Compared with evodiamine (2.0μmol·L -1 ) group,the protein expression levels of PI3K,p-AKT,PCNA,XI-AP and Survivin in SC79+evodiamine (2.0μmol·L -1 ) group were elevated （P＜0.05 or P＜0.01）,and the effects of evodiamine on inhibiting proliferation and inducing apoptosis of 5-8F cells decreased （P＜0.05 or P＜0.01）.Conclusion Evodiamine may inhibit proliferation and induce apoptosis of nasopharyngeal carcinoma cells by inhibiting the activity of PI3K/AKT signaling pathway and down-regulating the expression of proliferation and apoptosis-related proteins PCNA,XIAP and Survivin.

Background: The purpose of this study was to investigate the mechanism of sanguinarine (SAN) against nasopharyngeal carcinoma (NPC) by means of network pharmacology, molecular docking technique, and experimental verification. Methods: The SAN action targets were predicted using the Swiss Target Prediction database, the related NPC targets were determined using the GEO database, and the intersection of drug and disease pathway targets were considered to be the potential targets of SAN against NPC. The target-protein interaction network map was constructed using the STRING database, and the core target genes of SAN against NPC were obtained via topological network analysis. “R” language gene ontology (GO) function and Kyoto encyclopedia of genes and genome (KEGG) pathway enrichment analyses were used to dock the core target genes with SAN with the help of AutodockVina. Cell proliferation was detected using MTT and xCELLigence real-time cell analysis. Apoptosis was identified via Hoechst 33342 staining, JC-1 mitochondrial membrane staining, and annexin V-FITC/PI double fluorescence staining, while protein expression was quantified using western blotting. Results: A total of 95 SAN against NPC targets were obtained using target intersection, and 8 core targets were obtained by topological analysis and included EGFR, TP53, F2, FN1, PLAU, MMP9, SERPINE1, and CDK1. Gene ontology enrichment analysis identified 530 items, and 42 items were obtained by Kyoto encyclopedia of genes and genome pathway enrichment analysis and were mainly related to the PI3K/AKT, MAPK, and p53 signaling pathways. Molecular docking results showed that SAN had good binding activity to the core target. SAN inhibited the proliferation of NPC cells, induced apoptosis, reduced the expression levels of survivin and Bcl2, and increased the expression levels of Bax and cleaved caspase-8. It also decreased the expression levels of the key proteins p-c-Raf, p-MEK, and p-ERK1/2 in the MAPK/ERK signaling pathway in NPC cells. Conclusion: SAN inhibits the proliferation and induces the apoptosis of NPC cells through the MAPK/ERK signaling pathway.

To study the effect of berberine combined with formononetin on the migration of NPC cells, and to preliminarily explore the roles of the MAPK/ERK1/2 signaling pathway.Berberine combined with formononetin synergistically inhibited the proliferation, migration and invasion of NPC cells. After treatment, the expression of EMT-related proteins N-cadherin,vimentin and MAP4K4 decreased, that of E-cadherin increased, and that of p-c-Raf, p-MEK, p-ERK1/2 was down-regulated. After MAPK/ERK 1/2 signaling pathway was activated by EGF, the inhibitory effect of berberine combined with formononetin on the key proteins p-c-Raf, p-MEK, p-ERK1/2 of MAPK/ERK1/2 signaling pathway, and the downstream proteins N-cadherin and vimentin, and the promotion of E-cadherin were weakened. Meanwhile, the activation of MAPK/ERK1/2 signaling pathway reduced the inhibitory effect of berberine combined with formononetin on the migration of NPC cells.Berberine combined with formononetin decreases the activity of the MAPK/ERK1/2 signaling pathway, thus further inhibiting the migration of NPC cells.

Abstract Objectives: This study aims to analyze the expression and prognostic significance of chromobox (CBX) family genes in pan cancer and to associate their roles with immune subtypes, tumor microenvironment and drug sensitivity. Methods: TCGA +GTEX method was used to analyze five members of the CBX2/4/6/7/8, Using 11,093 samples from 33 tumor types in TCGA database，to multidimensional analysis of five members of the CBX family, CBX2, CBX4, CBX6, CBX7, CBX8.including the differential expression of the CBX family in pan cancer, as well as the correlation between immune subtypes, tumor purity and stemness.Finally, the correlation data of CellMiner database was used to analyze the relationship between CBXs and drug sensitivity. Then, GO plot was performed, and GSEA analysis and weighted gene co-expression network analysis were generated. CellMiner database was used to analyze the correlation and mechanism of CBX family genes with drug sensitivity. Results: CBX 2/4/8 were highly expressed in pan-cancers. The expression level of CBX6 was heterogeneous among different tumor types, while that of CBX7 was low. The results show that CBX2, CBX4, and CBX8 are highly expressed in pan-cancer,and CBX6 is heterogeneous among different tumor types, while CBX7 is lowly expressed in almost tumor types.The expression of CBXs was correlated with the overall survival of patients, but the correlation direction depended on the cancer type. CBXs were significantly correlated with immune infiltration subtypes (P< 0.001). The expression of CBX2/CBX7s had differences in stromal cell score and RNAss stemness score. High expression of CBX82 was correlated with the high purity of most types of cancers, while CBX7 was contrary to this pattern. Rich analysis indicated that CBXs may affect the occurrence and progression of tumors by regulating RNA splicing and transcription coactivator activity. The core genes of hsa-mir-181a and EGR1 were identified in the established mRNA-TF-miRNA WGCNA network. Finally, our study revealed that CBX2 gene may be associated with sensitivity to Acrichine, Curcumin, Nelarabine, Ixabepilone, Ifosfamide, tfdu and Tamoxifen.The high expression of CBX7 was positively correlated with the drug resistance of cells to Aminoflavone, AFP464 and Lificguat.Conclusion: The CBX family showed different expression in different tumor types. CBX2 acted as an oncogene and might be overexpressed in a variety of human cancers, and CBX7 acted as a tumor suppressor gene and might become a promising therapeutic target. This study revealed multiple expression patterns of CBXs in pan cancer, providing new insights for cancer treatment, but further laboratory validation is needed.

目的 基于Wnt/β-catenin信号通路探讨益气解毒方(黄芪、黄连、白花蛇舌草等)对鼻咽癌5-8F细胞凋亡的作用机制.方法(1)将5-8F细胞分为空白对照组、益气解毒方不同浓度组(0.25、0.5、1.0、2.0 mg·mL-1)及顺铂组(4 μg·mL-1),采用实时无标记细胞功能分析仪(RTCA)监测细胞的增殖情况.(2)将5-8F细胞分为5组:空白对照组、益气解毒方1.0 mg·mL-1组、HLY78 10 μmol·L-1组、HLY78 10 μmol·L-1+益气解毒方1.0mg·mL-1组、IWR-1 8μmol L-1组,采用RTCA监测细胞的增殖;药物干预36h后,采用Annexin V-FITC/PI双荧光染色法检测细胞凋亡率;JC-1荧光探针法检测细胞线粒体膜电位;Western Blot法检测细胞β-catenin、Wnt5a/b、Bcl2及Bax蛋白的表达水平.结果 与空白对照组比较,益气解毒方不同浓度组(0.25、0.5、1.0、2.0mg·mL-1)的5-8F细胞增殖曲线均明显降低;益气解毒方1.0mg·mL-1组、IWR-1 8 μmol·mL-1组的细胞凋亡率显著升高(P＜0.01),线粒体膜电位明显降低,β-catenin、Wnt5a/b及Bc12蛋白表达明显下调(P＜0.05,P＜0.01),Bax蛋白表达显著上调(P＜0.01),Bax/Bc12比值显著升高(P＜0.01).与益气解毒方1.0mg·mL-1组比较,HLY78 10μmol·L-1+益气解毒方1.0mg·mL-1组的5-8F细胞增殖曲线明显升高,细胞凋亡率显著下降(P＜0.01),线粒体膜电位明显升高,β-catenin、Wnt5a/b及Bc12蛋白表达明显上调(P＜0.05,P＜0.01),Bax蛋白表达显著下调(P＜0.01),Bax/Bc12比值显著降低(P＜0.01).结论 益气解毒方能够抑制鼻咽癌5-8F细胞增殖,并诱导细胞凋亡,其机制与抑制Wnt/β-catenin信号通路相关.

Objective To predict the molecular mechanisms behind the benefits of Scutellaria barbata D. Don (S. barbata) in nasopharyngeal carcinoma (NPC) by network pharmacology and experimental verification. Methods The active ingredients and targets of S. barbata were searched in the traditional Chinese medicine system pharmacology database and analysis platform, and the disease targets of NPC were obtained by searching the GeneCards database. A common target protein-protein interaction network was constructed by STRING, and then, an active ingredients-NPC-target interaction network map was constructed by Cytoscape 3.7.2 software. The functional enrichment analyses of Gene Ontology and KEGG pathway data were carried out by R software programming. Finally, cell proliferation was assessed by CCK8, apoptosis was detected by Annexin V-FITC/PI double fluorescence staining, and protein expression was analyzed by Western blotting. Results In this study, 29 active ingredients were found in S. barbata. Among these, the main targets for NPC were baicalein, wogonin, luteolin, and quercetin. The main molecular targets of S. barbata on NPC were EGFR, MYC, CASP3, CCND1, and ESR1. The main biological processes involved the binding of DNA-binding transcription factors, RNA polymerase II-specific DNA-binding transcription factors, ubiquitin-like protein ligases, and ubiquitin-protein ligases. S. barbata mainly affects NPC through the PI3K-Akt, p53, and MAPK signaling pathways. The experimental results showed that baicalein and wogonin could inhibit proliferation and induce apoptosis of NPC cells and downregulate the expression of PI3K, AKT, and p53, the key proteins of the PI3K/AKT and p53 signaling pathway in CNE2 cells. Conclusion Baicalein and wogonin, the main active ingredients of S. barbata, inhibited the proliferation and induced apoptosis of NPC cells through the PI3K/AKT and p53 signaling pathways.

目的 研究小檗碱联合芒柄花黄素对鼻咽癌细胞迁移的影响,探讨转化生长因子-β1(transforming growth factor-β1,TGF-β1)信号通路在其效应中的作用.方法 采用实时无标记细胞功能分析仪监测小檗碱和芒柄花黄素单用及联合使用对鼻咽癌5-8F、6-10B细胞增殖的影响;采用划痕实验和Transwell实验检测TGF-β1信号通路激活后,小檗碱联合芒柄花黄素抑制细胞迁移效应的变化;采用Western blotting检测TGF-β1信号通路关键蛋白和迁移相关蛋白的表达.结果 与对照组比较,小檗碱和芒柄花黄素单用可抑制5-8F和6-10B细胞增殖,小檗碱(5、10 μmol/L)和芒柄花黄素(5、10 μmol/L)联合作用于5-8F和6-10B细胞后,显示小檗碱联合芒柄花黄素抑制鼻咽癌细胞增殖以协同效应为主;小檗碱联合芒柄花黄素显著降低鼻咽癌细胞TGF-β1和Smad3蛋白表达水平(P＜0.05、0.01).采用TGF-β1激活TGF-β1信号通路后,小檗碱联合芒柄花黄素抑制鼻咽癌细胞迁移的效应显著降低(P＜0.01);与小檗碱10μmol/L+芒柄花黄素10μmol/L组相比,TGF-β1+小檗碱+芒柄花黄素组细胞 TGF-β1、Smad3、磷酸化细胞外调节激酶 1/2(phosphorylated extracellular signal regulated kinase 1/2,p-ERK1/2)蛋白表达水平显著上调(P＜0.05、0.01),N-钙黏蛋白(N-cadherin)、波形蛋白(vimentin)表达水平升高,E-钙黏蛋白(E-cadherin)表达水平降低(P＜0.01).结论 小檗碱联合芒柄花黄素能够协同抑制鼻咽癌细胞迁移,其作用机制可能与抑制TGF-β1信号通路有关.

目的 探讨黄芩苷(baicalin)对鼻咽癌CNE2细胞增殖及TGF-β1/ERK1/2信号通路的作用.方法 采用CCK8法检测不同浓度黄芩苷(2.5、5、10、20、40、80μmol·L-1)、顺铂(4μg·mL-1)在24、36、48 h对CNE2细胞增殖的作用;细胞成像多功能检测系统(CytationTM 5)实时监测黄芩苷对CNE2增殖数量的变化;Western blot检测黄芩苷对CNE2细胞增殖相关蛋白PCNA、Survivin及TGF-β1/ERK1/2信号通路关键蛋白TGF-β1、p-ERK1/2的影响.结果 CCK8结果显示,黄芩苷可抑制CNE2增殖(P<0.05或P<0.01),且随着浓度升高,抑制作用增强;CytationTM 5监测结果显示,黄芩苷可抑制CNE2细胞数量增多(P<0.05或P<0.01);Western blot结果表明,黄芩苷下调了增殖相关蛋白PCNA(P<0.05)、Survivin(P<0.05)及TGF-β1/ERK1/2信号通路关键蛋白TGF-β1(P<0.05)、p-ERK1/2(P<0.05)的表达水平.加入TGF-β1(TGF-β1/ERK1/2信号通路激活剂)后,黄芩苷对TGF-β1、p-ERK1/2、PCNA、Survivin的抑制作用降低(P<0.05),同时降低了黄芩苷对CNE2细胞增殖的抑制作用.结论 黄芩苷能够抑制鼻咽癌CNE2细胞增殖,并通过抑制TGF-β1/ERK1/2信号通路进一步降低下游蛋白PCNA、Survivin的表达发挥作用.

Objective: To study the biological behavior of nasopharyngeal carcinoma stem cells and to explore the activation of Ras signaling pathway regulated by CD44. Methods: CNE2-SC and 5-8F-SC were nasopharyngeal carcinoma stem cells and obtained by serum-free suspension culture. Cell counting kit-8 (CCK-8) assay, colony formation assay, Transwell migration assay, cell adhesion array were used to investigate the growth, proliferation, migration and adhesion of nasopharyngeal carcinoma stem cells. Western blot test was used to detect the expressions of Ras signaling pathway related proteins and siRNA-mediated interference was used to determine the activation of Ras signaling pathway regulated by CD44. Results: The growth rates of CNE2-SC and 5-8F-SC cells were significantly lower than those of nasopharyngeal carcinoma cells at 24, 48 and 72 hours after inoculation (P<0.05). After 14 days of implantation, the colony formation rates of CNE2-SC (44.5±1.9)% and 5-8F-SC (47.4±1.8)% were higher than those of CNE2 (34.9±1.5)% and 5-8F (37.2±1.7)%, respectively(P<0.01). The migration cell number of CNE2-SC was (87.6±7.8), 3.97 times higher than that of CNE2 (P<0.01). The migration cell number of 5-8F-SC was (67.2±5.7), 3.07 times higher than 5-8F (P<0.01). The adhesion rates of CNE2-SC and CNE2 cells were (42.1±7.6)% and (8.9±2.0)%, respectively at 3 hours after inoculation and were (82.4±5.0)% and (12.1±2.2)% at 6 hours after inoculation, respectively. The adhesion rate of CNE2-SC cells was higher than that of CNE2 cells (all P<0.01). The adhesion rates of 5-8F-SC and 5-8F cells were (53.6±6.1)% and (7.3±1.5)% at 3 hours after inoculation, and (90.7±3.6)% and (11.0±1.2)% at 6 hours after inoculation, respectively. The adhesion rate of 5-8F-SC cells was higher than that of 5-8F cells (P<0.01). The expression levels of CD44, Ras and N-cadherin were significantly higher, while phosphatase and tensin homolog deleted on chromosome 10 (PTEN), E-cadherin in nasopharyngeal carcinoma stem cells were lower than those of the nasopharyngeal carcinoma cells. Furthermore, the levels of phosphorylated mitogen extracellular kinase1/2 (p-MEK1/2) and phosphorylated extracellular signal-regulated protein kinase1/2 (p-ERK1/2)were significantly increased in nasopharyngeal carcinoma stem cells (P<0.01). Correlation analysis showed that the protein expression levels of CD44 was highly positively correlated with RAS in nasopharyngeal carcinoma stem cells(r=0.985, P=0.002; r=0.962, P=0.038). Deletion of CD44 in CNE2-SC decreased the expression levels of HER-2, Ras and p-ERK1/2, p-Akt and phosphorylated protein kinase C-δ(p-PKCδ) (P<0.01). Conclusions: Despite compare to the nasopharyngeal carcinoma cell, nasopharyngeal carcinoma stem cells grows at a relatively slow rate, the capacities of clone formation, migration, adhesion are promoted. This may be related to the CD44-regulated abnormal activation of Ras signaling pathway.

目的:探讨益气解毒方对鼻咽癌细胞自噬的影响及其机制.方法:MTT检测益气解毒方对鼻咽癌CNE-2Z细胞增殖的影响.透射电镜和MDC染色观察益气解毒方诱导CNE-2Z细胞的自噬效应.Western Blot法检测Beclin-1、LC3、PI3K、p-AKT和p-mTOR蛋白表达量.结果:益气解毒方抑制CNE-2Z细胞增殖(P＜0.05,P＜0.01).与对照组比较,不同浓度益气解毒方组细胞内出现自噬体、MDC荧光强度增加、Beclin-1和LC3Ⅱ蛋白表达上调(P＜0.05,P＜0.01),其中0.5mg/mL益气解毒方组增加最明显.与0.5mg/mL益气解毒方组比较,0.5mg/mL益气解毒方+3-MA组MDC荧光强度、Beclin-1和LC3Ⅱ蛋白降低(P＜0.05).与对照组比较,0.5mg/mL和1mg/mL益气解毒方组的PI3K、p-AKT和p-mTOR的蛋白表达均出现下调(P＜0.05).结论:益气解毒方可诱导鼻咽癌CNE-2Z细胞自噬,其机制可能是通过激活PI3K/AKT/mTOR信号通路.

目的 评价中医推拿治疗急性乳腺炎的临床疗效,从而为临床治疗提供可靠的循证医学依据.方法 在中国知识资源总库(CNKI),维普期刊资源数据库(VIP),中国学术期刊数据库(万方数据库)检索2014～2019年收录的中医推拿治疗急性乳腺炎的文献,2名研究者独立进行全文阅读,根据纳入及排除标准等相关标准筛选出10篇文献纳入研究,再资料提取,文献质量评价后,对结局指标,样本量通过Revman5.2软件进行数据分析处理.结果 纳入10篇文献,患者例数1222例;Meta分析,异质性检测P=0.98,I2 =0％,说明纳入的文献研究之间具有同质性,采用固定效应模型检測分析.结果显示:观察组与对照组差异有统计学意义,OR=3.73,95％CI=[2.51,5.55],Z=5.55,P＜0.00001,说明观察组治疗效果优于对照组.结论 中医推拿治疗急性乳腺炎的临床疗效优于对照组,但纳入的文献亦有不足,如文献数量比较少,文献质量不高,文献样本数量偏少,及文献样本量范围局限等;中医推拿治疗急性乳腺炎的临床疗效验证需要更多大量本、多中心研究及高质量的文献数据来支持.

目的:观察益气解毒方联合盐霉素对鼻咽癌干细胞增殖的影响并初步探讨其分子机制.方法:益气解毒方、盐霉素(SAL)单独或联合干预鼻咽癌干细胞CNE2-SC、5-8F-SC后,细胞计数法、平板克隆形成试验观察其增殖和克隆形成能力,Western Blot法检测相关蛋白的表达水平.结果:益气解毒方和SAL均显著抑制鼻咽癌干细胞增殖且呈现出浓度依赖性.各药物组均能显著抑制鼻咽癌干细胞增殖和克隆形成(P＜0.01),且益气解毒方+SAL抑制效应更强.益气解毒方组及益气解毒方+SAL组CNE2-SC和5-8F-SC的XIAP、Survivin、ALDH1/2表达水平显著降低(P＜0.01).SAL组CNE2-SC细胞ALDH1/2表达水平显著下降(P＜0.01),但XIAP、Survivin表达水平显著升高(P＜0.01);5-8F-SC细胞ALDH1/2、Survivin表达水平显著降低(P＜0.01),但XIAP表达水平无明显变化.结论:益气解毒方联合盐霉素具有协同抑制鼻咽癌干细胞增殖的效应,其机制可能与其下调鼻咽癌干细胞中生存相关蛋白XIAP和Survivin以及干性相关蛋白ALDH1/2的表达相关.

Objective To assess the effects of Yi Qi Jie Du Decoction (YQJDD) on nasopharyngeal carcinoma stem cells (NPC-SCs) and investigate the underlying mechanism. Methods NPC-SCs were collected in serum-free culture system and identified by the sphere formation assay. The effect of YQJDD on the proliferation of NPC-SCs was detected using the Cell Counting Kit-8 assay. The change of mitochondrial membrane potential (ΔΨm) in NPC-SCs following treatment with YQJDD was investigated by JC-1 staining. The levels of apoptosis-associated proteins were examined using western blot analysis. Results YQJDD significantly inhibited the proliferation of NPC-SCs in dose- and time-dependent manners. JC-1 staining revealed that YQJDD lowered the ΔΨm of NPC-SCs in a time-dependent manner. After treatment with YQJDD, the expression of cleaved caspase-3, -7 and -9, cleaved poly-ADP ribose polymerase, P21 and P53 were increased, while the expression of Survivin in NPC-SCs was decreased. However, the expression of cleaved caspase-8 remained nearly unchanged. Conclusions YQJDD inhibits the growth and induces apoptosis of NPC-SCs via an intrinsic apoptosis pathway.

目的 研究鼻咽癌干细胞的增殖特征并初步探讨其分子机制.方法 采用无血清悬浮培养法从鼻咽癌细胞CNE2和5-8F获得鼻咽癌干细胞CNE2-SC、5-8F-SC,分别采用细胞存活率分析计数器、细胞平板克隆形成试验观察鼻咽癌干细胞的增殖特性和克隆形成能力,Western blot法检测细胞周期相关蛋白表达水平.结果 鼻咽癌干细胞比其来源的鼻咽癌细胞增殖速度显著降低,差异有统计学意义(P＜0.05).鼻咽癌干细胞克隆形成率显著高于其来源鼻咽癌细胞(P＜0.01),但肿瘤干细胞克隆显著小于其来源细胞.与普通鼻咽癌细胞比较,鼻咽癌干细胞的细胞周期蛋白CylinD1、CylinD3及细胞周期调控蛋白CDK2、CDK4、CDK6的表达水平显著下调(P＜0.01).结论 鼻咽癌干细胞比其来源的鼻咽癌细胞生长增殖缓慢,可能与其细胞周期蛋白和周期蛋白依赖激酶表达水平下调有关.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的研究益气解毒方水提物对鼻咽癌细胞凋亡的影响,并从MAPK/ERK信号通路探讨其诱导凋亡的作用机制。方法 CCK-8法检测益气解毒方水提物对CNE1、CNE2细胞增殖的影响;Hoechst 33342染色法、JC-10染色法、荧光双染流式细胞仪检测其对CNE1、CNE2细胞凋亡的影响;Western blot法检测其对CNE1、CNE2细胞蛋白表达的影响。结果益气解毒方水提物能抑制CNE1、CNE2细胞增殖（P&lt;0.05）、诱导凋亡（P&lt;0.05）;药物作用48 h后,Survivin、XIAP、Bcl-2表达下降,Bax表达上升,MAPK/ERK信号通路关键蛋白p-c-Raf、p-MEK、p-ERK表达下降（P&lt;0.05）;在此基础上,加入激活剂ISO和益气解毒方水提物后,与单用益气解毒方水提物相比,p-c-Raf、p-MEK、p-ERK1/2表达上调,Survivin、XIAP、Bcl-2表达增加,Bax表达下降,促凋亡效应也降低（P&lt;0.05）。结论益气解毒方水提物可诱导鼻咽癌细胞凋亡,该效应与其抑制MAPK/ERK信号通路关键蛋白p-c-Raf、p-MEK、p-ERK1/2表达,进而下调Survivin、XIAP、Bcl-2表达,上调Bax表达有关。</span>

通过影视剧、教材、临床三种途径收集护患沟通素材,制作护理人际沟通情境资源.尝试将情境资源应用于护理人际沟通的课堂教学中,通过课堂体验、课后讨论等方式,将理论知识与临床实践有机结合,进一步丰富教学形式,提高教学效率,从而达到激发学习积极性,提高实际沟通能力的效果,同时提高教师自身的综合素质.

目的:观察中医推拿对早期外吹乳痈的护理效果.方法:选择80名早期外吹乳痈患者,随机分为治疗组与对照组各40例,治疗组采用中医推拿结合肌腱线疏通的方法进行干预,对照组采用抗生素进行干预,疗程均为5天.观察两组的症状体征积分改善情况、治疗效果及1月后的复发率和母乳喂养率.结果:治疗组症状体征积分明显降低,与对照组比较差异有统计学意义(P＜0.05);两组疗效结果比较,治疗组优于对照组(P＜0.05);一月后两组复发率比较无明显差异(P＞0.05),母乳喂养率治疗组优于对照组(P＜0.05).结论:中医推拿对早期外吹乳痈有着较好疗效,且优于抗生素治疗,其对于维持和促进母乳喂养有着积极意义.