益生菌联合抗幽门螺杆菌治疗对 消化性溃疡患者的疗效

目的探讨益生菌联合抗幽门螺杆菌(H.pylori)治疗对消化性溃疡患者的疗效及其对患者肠道菌群的影响。方法将120例经14 C呼气试验(14 C-UBT)检测确定为H.pylori感染阳性的消化性溃疡患者随机分为观察组和对照组,每组60例。其中,对照组采用四联疗法(奥美拉唑+阿莫西林+克拉霉素+铋剂)治疗,观察组采用四联疗法联合益生菌治疗;比较两组患者H.pylori根除情况、溃疡愈合质量及不良反应情况。治疗前后留取全部患者的新鲜粪便标本进行细菌培养,比较两组患者肠道菌群数量和肠道微生物定植抗力(B/E值)。结果观察组患者H.pylori根除率和溃疡愈合率分别为88.3%、95.0%,显著高于对照组的70.0%和76.7%(P0.05),不良反应率为3.3%,显著低于对照组的20.0%(P0.05)。与治疗前比,对照组患者治疗后肠道内产气荚膜梭菌、双歧杆菌及乳杆菌数量显著减少(P0.05),肠杆菌、肠球菌及酵母菌数量显著增加(P0.05),B/E值显著降低(P0.05);观察组患者治疗后双歧杆菌和乳杆菌数量均显著增加(P0.05),产气荚膜梭菌数量显著减少(P0.05),肠杆菌、肠球菌及酵母菌数量无明显变化(P0.05),B/E值显著升高(P0.05)。结论常规抗H.pylori治疗易引起消化性溃疡患者肠道菌群紊乱,降低肠道定植抗力。益生菌联合治疗可有效改善患者肠道微生态,提高H.pylori根除率和溃疡愈合质量,减少不良反应。     

FBXW7 suppresses epithelial‐mesenchymal transition and chemo‐resistance of non‐small‐cell lung cancer cells by targeting snai1 for ubiquitin‐dependent degradation

Objectives

FBXW7 acts as a tumour suppressor by targeting at various oncoproteins for ubiquitin‐mediated degradation. However, the clinical significance and the involving regulatory mechanisms of FBXW7 manipulation of NSCLC regeneration and therapy response are not clear.

Materials and Methods

Immunohistochemical staining and qRT‐PCR were applied to detect FBXW7 and Snai1 expression in 100 samples of NSCLC and matched tumour‐adjacent tissues. FBXW7 manipulation of cancer biological functions were studied by using MTT assay, immunoblotting, flow cytometry, transwells, wound healing assay, and sphere‐formation assays. Immunofluorescence and co‐immunoprecipitation were used to analyse the possible interaction between Snai1 and FBXW7.

Results

We detected the decreased FBXW7 expression in majority of the NSCLC tissues, and lower FBXW7 level was correlated with advanced TNM stage. Furthermore, those patients with decreased FBXW7 expression tend to have both poorer 5‐year survival outcomes, and shorter disease‐free survival, comparing to those with higher FBXW7 levels. Functionally, we found that FBXW7 enforcement suppressed NSCLC progression by inducing cell growth arrest, increasing chemo‐sensitivity and inhibiting Epithelial‐mesenchymal Transition (EMT) progress. Results further showed that FBXW7 could interact with Snai1 directly to degrade its expression through ubiquitylating alternation in NSCLC, which could be partially abrogated by restoring Snai1 expression.

Conclusions

FBXW7 conduction of tumour suppression was partly through degrading Snai1 directly for ubiquitylating regulation in NSCLC

     

Influence of a dosing-time on toxicities induced by docetaxel,cisplatin and 5-fluorouracil in patients with oral squamous cell carcinoma; a cross-over pilot study

Docetaxel, cisplatin plus fluorouracil (DCF) regimen is a useful chemotherapy, but is sometimes withdrawn due to severe adverse effects (AE). In this study, we examined whether the chronotherapy of DCF regimen could reduce the drugs-induced toxicities in clinical practice. Patients with oral squamous cell carcinoma were enrolled. Chemotherapy started at 10:30 (Morning-dosing) or 18:30 (Evening-dosing) for 5 days by a cross-over design. AE were assessed for 14 days after an initiation of each dosing. The grades of nausea, vomiting and neutropenia were smaller during Evening-dosing than during Morning-dosing. These data suggest that the chrono-chemotherapy might provide a merit for reducing the DCF regimen-related severe AE.     

Adoptive transfer of natural killer cells in combination with chemotherapy improves outcomes of patients with locally advanced colon carcinoma

Background

Despite the availability of multiple treatment strategies, patients with advanced colon carcinoma (CC) have poor prognoses. The aim of this study was to evaluate the efficacy and safety of natural killer (NK) cell therapy in combination with chemotherapy in patients with locally advanced CC.

光动力抗微生物化学疗法对解脲脲原体体外活性的影响

解脲脲原体是一种重要的病原微生物,近年来其耐药形势十分严峻,因此寻找一种全新的有效替代治疗方案尤为重要。本研究旨在探索光动力抗微生物化学疗法对解脲脲原体体外活性的影响。选取解脲脲原体两种生物群（Parvo生物群及T960生物群）代表菌株,包括标准株及临床株,与系列稀释的2.5~0.039 062 5 mmol/L光敏剂甲苯胺蓝孵育20 min或60 min,再以（633±10）nm红光照射,设置48、102、204和408 mJ/cm²共4组能量密度,48 h后判读结果。观察不同解脲脲原体与甲苯胺蓝孵育时间、甲苯胺蓝浓度、光照能量密度对光动力抗微生物化学疗法灭活解脲脲原体效果的影响,并观察两种生物群对光动力抗微生物化学疗法敏感性的差异。结果显示,光动力抗微生物化学疗法在体外对解脲脲原体有明显灭活作用。在光照能量密度及解脲脲原体与甲苯胺蓝孵育时间固定的前提下,这种灭活作用随甲苯胺蓝浓度的增加而增强;单一633 nm红光光源在408 J/cm²及以下的能量密度对解脲脲原体的活性无明显影响。在甲苯胺蓝浓度及解脲脲原体与甲苯胺蓝孵育时间固定的条件下,光动力抗微生物化学疗法对解脲脲原体的灭活作用随光照能量密度（48~408 mJ/cm²）的增加而增强;随甲苯胺蓝孵育时间（30~60 min）延长,光动力抗微生物化学疗法对解脲脲原体的灭活作用有增强的趋势。结果提示,解脲脲原体两种生物群对光动力抗微生物化学疗法的敏感性相似。本研究证实,光动力抗微生物化学疗法在体外能有效灭活解脲脲原体,有望成为解脲脲原体感染的有效替代治疗方法。     

重组人血管内皮抑素用于骨肉瘤术后化疗的疗效及对VEGF、PCNA、PTEN的影响

目的:研究重组人血管内皮抑素用于骨肉瘤术后化疗的疗效及对血管内皮生长因子(VEGF)、增殖细胞核抗原(PCNA)、第10染色体丢失的磷酸酶(PTEN)的影响。方法:收集2014年3月至2016年3月我院的220例骨肉瘤患者,按抽签法分为实验组和对照组,每组各110例。对照组采用DIA化疗方案治疗,静脉滴注顺铂、异环磷酰胺、阿霉素。实验组在对照组基础上,采用重组人血管内皮抑素治疗,每次15 mg静脉滴注。两组均治疗2个疗程。对比两组治疗疗效,肢体功能评价,VEGF、PTEN水平,PCNA阳性表达率,不良反应发生率。结果:实验组总有效率显著高于对照组[81.81%(90/110)vs65.45%(72/110)](P0.05);实验组肢体功能优良率显著高于对照组[79.09%(87/110)vs63.63%(70/110)](P0.05);两组PTEN水平较治疗后显著升高,但无差异(P0.05),两组VEGF水平较治疗后显著降低,且实验组低于对照组(P0.05);两组PCNA阳性表达率较治疗前显著降低,且实验组低于对照组(P0.05);两组不良反应发生率无差异(P0.05)。结论:重组人血管内皮抑素在骨肉瘤术后化疗中的效果显著,可调节血管内皮细胞平衡,降低VEGF水平以及PCNA阳性表达率,减少细胞增殖,提高PTEN水平,增强抑制恶性肿瘤细胞作用。     

喜树碱-氟尿苷纳米颗粒对口腔鳞癌细胞Tca-8113增殖与迁移的影响

目的:探究喜树碱-氟尿苷(CPT-FUDR)纳米颗粒对口腔鳞癌Tca-8113细胞增殖与迁移的影响。方法:制备喜树碱-氟尿苷纳米颗粒,通过丁达尔现象证明已组装完毕。将制备好的纳米颗粒组和喜树碱(CPT)单药组、氟尿苷(FUDR)单药组以及两种单药混合组(CPT/FUDR)作对比,采用MTT实验检测药物对口腔鳞癌细胞Tca-8113增殖的抑制作用,通过划痕实验探究CPT-FUDR纳米颗粒和CPT/FUDR混合药物对细胞迁移能力的影响。结果:MTT结果显示:在药物浓度大于0.1μM时,随着浓度的增加,四组细胞存活率均明显下降(P0.05),而CPT-FUDR纳米颗粒组Tca-8113细胞的存活率明显低于单药CPT、FUDR和CPT/FUDR混合物组(P0.05)。在划痕实验中,培养48 h后,CPT/FUDR混合物组和CPT-FUDR纳米颗粒组均显著低于空白组(P0.05),且CPT-FUDR纳米颗粒组显著低于CPT/FUDR混合物组(P0.05)。结论:在体外,CPT-FUDR纳米颗粒对口腔鳞癌Tca-8113细胞的增殖与迁移有较好的抑制作用,且抑制效果优于CPT/FUDR两种单药混合。     

The cytotoxic interaction of inorganic trace elements with EDTA and cisplatin in sensitive and resistant human ovarian cancer cells

Summary Cisplatin (CDDP)-sensitive and -resistant human ovarian cells were studied in vitro with the objective of enhancing CDDP cytotoxicity by the addition of a metal and the chelate ethylenediaminetetraacetic acid (EDTA), to the CDDP. Chelateable elements, such as bismuth, calcium, cadmium, copper, iron, magnesium, selenium, vanadium, and zinc, when added to CDDP and in the presence of EDTA increased the cytotoxicity of the CDDP as compared to CDDP treatment alone.