双参颗粒散剂及水煎剂入血成分差异的初步分析

目的:初步分析大鼠口服双参颗粒散剂与水煎剂后的入血成分差异。方法:采用LC/MS-IT-TOF方法对双参颗粒醇提取物、水提取物含药血清、散剂含药血清进行分析,根据保留时间、精确相对分子质量,质谱数据等完成各组成分差异比较。结果:和水煎剂比较,初步鉴定出双参颗粒散剂特有的4个原型吸收入血成分,分别是Ginsenoside-Rh1,Ginsenoside-Rg2,Ginsenoside-Rb2和Ginsenoside-Rg3。结论:双参颗粒散剂和水煎剂在大鼠入血成分存在差异,这些入血成分可能是双参颗粒散剂异于水煎剂在血中起直接作用的物质。     

平均床值法摆位技术在颈椎骨转移瘤调强放疗中的应用研究

目的 运用千伏级的锥形束CT（cone beam CT,CBCT）图像引导扫描技术,研究平均床值法摆位技术在颈椎骨转移瘤调强放疗中应用的可行性。方法 每位患者总共扫描30次CBCT,记录每次左右方向x、前后方向y、上下方向z三个方向的数值,取前5次CBCT扫描平均值x₅=（x₁+x₂+…x₅）/5,y₅=（y₁+y₂+…y₅）/5,z₅=（z₁+z₂+…z₅）/5,作为日后摆位床值,与物理师的计划床值x₀、y₀、z₀进行分析,前5次左右方向摆位平均误差Lat₅=x₅-x₀,前后方向摆位平均误差Lng₅=y₅-y₀,上下方向摆位平均误差Vrt₅=z₅-z₀,用前5次摆位误差的平均值表示系统误差,用所有分次的摆位误差的标准差表示随机误差,进行独立t检验。结果 平均床值法摆位技术的系统误差和随机误差无显著性差异（P>0.05）,在左右、前后、上下三个维度的误差都<0.3 cm,在允许范围内。结论 平均床值法摆位技术运用在颈椎骨转移瘤的调强放疗是可行的。     

依西美坦和阿那曲唑在乳腺癌内分泌治疗中不良反应差异的分析

目的:探讨乳腺癌患者常用非甾体类芳香化酶抑制剂阿那曲唑和甾体类芳香化酶抑制剂依西美坦在不良反应方面的差异。方法:检索PubMed、中国知识资源总库、CNKI、万方数据库中提供依西美坦和阿那曲唑不良反应的随机对照临床试验，对符合标准的文献提取相关不良反应指标，应用RevMan 5.3软件进行Meta分析。结果:纳入5项研究，荟萃分析结果显示阿那曲唑和依西美坦在导致潮热、乏力、高血压、关节炎或关节痛方面无显著差异，而应用依西美坦高甘油三酯血症的发生率比阿那曲唑少19％（OR=0.81,95％CI:0.69~0.94;P=0.005)，高胆固醇血症的发生率比阿那曲唑少17％(OR=0.83，95％CI:0.76~0.92;P=0.000 3)，差异有统计学意义。结论:依西美坦比阿那曲唑较少引起高甘油三酯血症和高胆固醇血症，对于有高甘油三酯血症或高胆固醇血症患者及其他心血管疾病高危因素的患者，依西美坦可能是更好的选择。     

柱前衍生化HPLC法测定加巴喷丁胶囊中主药的含量

目的:建立柱前衍生化HPLC法测定加巴喷丁胶囊中的主药含量。方法:对加巴喷丁柱前衍生化后进行测定,选择Sinochrom-ODS(250 mm×4.6 mm,5μm)为固定相,0.33 mol.L-1乙酸水溶液-甲醇-乙腈(30∶70∶30)为流动相等度洗脱,流速1.0 mL.min-1,检测波长336 nm。结果:加巴喷丁在1.0～12.0 mg.L-1质量浓度范围内线性关系良好,其平均加样回收率为99.4%(n=9),RSD为0.84%;测得样品中加巴喷丁含量为标示量的99.82%。结论:该法便捷可靠,专属性强,可用于加巴喷丁胶囊中主药的含量测定。     

周维顺教授运用中医药治疗食管癌经验

介绍周维顺教授对食管癌的认识、诊断、临床用药治疗和预防的经验。     

Src激酶在骨肉瘤U2OS细胞失巢凋亡中的作用

【摘要】 目的 探讨Src激酶在骨肉瘤U2OS细胞失巢凋亡中的作用。方法 采用超低黏附板构建骨肉瘤U2OS细胞失巢凋亡抵抗模型,Western blot检测骨肉瘤U2OS细胞和失巢凋亡抵抗细胞中Src激酶蛋白的水平。加入Src激酶抑制剂,Western blot检测U2OS细胞中Src激酶蛋白的水平变化,并利用TUNEL染色和流式细胞双染技术检测细胞凋亡率。结果 成功构建骨肉瘤失巢凋亡抵抗模型细胞（U2OSar）,在骨肉瘤失巢凋亡过程中,p Src的蛋白水平逐渐升高;与骨肉瘤U2OS细胞相比,U2OSar细胞中,p Src/Src蛋白灰度比值023上升至091（P＜005）;加入Src激酶抑制剂PP2后, 骨肉瘤U2OS细胞的p Src的蛋白水平明显降低,凋亡率从4666%下降至2832%（P＜005）。结论 Src激酶参与调控骨肉瘤失巢凋亡,抑制肿瘤细胞凋亡,促进其失巢凋亡抵抗。     

Hub gene target of glioblastoma: LOX,SERPINH1 and TGFBI

Glioblastoma (GBM) is a malignant tumor. The long-term prognosis of the patients is poor. Therefore, it is of important clinical value to further explore the pathogenesis and look for molecular markers for early diagnosis and targeted treatment. Two expression profiling datasets [{"type":"entrez-geo","attrs":{"text":"GSE50161","term_id":"50161"}}GSE50161 ({"type":"entrez-geo","attrs":{"text":"GPL570","term_id":"570"}}GPL570 platform), {"type":"entrez-geo","attrs":{"text":"GSE116520","term_id":"116520"}}GSE116520 ({"type":"entrez-geo","attrs":{"text":"GPL10558","term_id":"10558"}}GPL10558 platform)] were respectively downloaded from the gene expression omnibus database. Volcano diagrams show the Differently expressed genes (DEGs) of {"type":"entrez-geo","attrs":{"text":"GSE50161","term_id":"50161"}}GSE50161 and {"type":"entrez-geo","attrs":{"text":"GSE116520","term_id":"116520"}}GSE116520. A Venn diagram revealed 467 common DEGs between the 2 datasets. Lysyl oxidase (LOX), serpin family H member 1 (SERPINH1) and transforming growth factor beta induced (TGFBI) were negatively correlated with the overall survival rate in patients with GBM. The hub genes are high in GBM tumor tissues. The relative expression levels of LOX, SERPINH1 and TGFBI were significantly higher in GBM samples, compared with the normal brain tissues groups. Bioinformatics technology could be a useful tool to predict progression of GBM and to explore the mechanism of GBM.LOX, SERPINH1 and TGFBI may be involved in the mechanism of the occurrence and development of GBM, and may be used as molecular targets for early diagnosis and specific treatment.DEGs identified using GEO2R. Functional annotation of DEGs using Kyoto Encyclopedia of Genes and Genomes and gene body pathway enrichment analysis. Construction of a protein-protein interaction network. The pathway and process enrichment analysis of the hub genes were performed by Metascape. Survival analysis was performed in gene expression profiling interactive analysis. Real-time fluorescent quantitative polymerase chain reaction assay was performed to verify. The animal model was established for western blot test analysis.     

Downregulation of microRNA-23a suppresses prostate cancer metastasis by targeting the PAK6-LIMK1 signaling pathway

Here we found that levels of miR-23a were decreased in prostate cancer cell lines and tumor tissues. These low levels were associated with poor patients'' prognosis. MiR-23a inhibited migration and invasion of prostate cancer in vivo and in orthotopic prostate cancer mice model. MiR-23a decreased levels of p21-activated kinase 6 (PAK6). Expression of miR-23a inhibited phosphorylation of LIM kinase 1 (LIMK1) and cofilin, in turn suppressing formation of stress fibers and actin filaments, which was required for cell motility and invasion. PAK6 bound to LIMK1 and activated it via phosphorylation at Thr-508. Also, PAK6 and LIMK1 were colocalized in the cytoplasma. Thus, miR-23a regulated cytoskeleton by affecting LIMK1 and cofilin. In summary, we have identified the miR-23a-PAK6-LIMK1 pathway of prostate cancer metastasis. Potential therapeutic approach by targeting miR-23 is suggested.     

Gut microbiota and lipid metabolism alterations in mice induced by oral cadmium telluride quantum dots

The potential toxicity of cadmium-containing quantum dots (QDs) has received much attention because of increasing biomedical applications. However, little has been known about how cadmium telluride (CdTe) QDs influence the gut microbiota and lipid metabolism. In this study, mice were exposed orally to CdTe QDs (200 μL of 0.2, 2, 20 or 200 μm ; twice per week) for 4 weeks. The oral experiments showed CdTe QD exposure led to a decrease of the Firmicutes/Bacteroidetes (F/B) ratio of gut microbiota, which highly negatively correlated with the low-density lipoprotein (LDL), triglyceride (TG) and total cholesterol (TC) levels in serum. In addition, the low-dose (0.2 and 2 μm ) CdTe QDs significantly increased the diversity of gut microbiota, and did not elevate the LDL, TG and TC levels in serum. The medium dose (20 μm ) of CdTe QDs caused the biggest decrease of the F/B ratio, so it significantly increased the LDL, TG and TC levels compared with the control. Furthermore, high-dose (200 μm ) CdTe QDs caused various toxicities in the histopathology of liver and intestine, liver function and intestinal immunity, but did not significantly lead to changes of the LDL, TG and TC levels in serum. This study demonstrates that high-dose oral CdTe QDs mainly lead to tissue damage of the liver and intestine, while the medium and low doses of oral CdTe QDs induce shifts of gut microbiota structure, which are associated with blood lipid levels.