两种不同方案治疗晚期非小细胞肺癌的疗效比较(英文)

Objective: The aim of this study was to analyze and compare the recent efficacy and toxicity of a three-drug platinum-based regimen (A regimen): [cisplatin (DDP) + gemcitabine (GEM) + vinorelbine (NVB)] and a two-drug combination without a platinum drug (B regimen): GEM + NVB, which were used to treat 55 advanced non-small cell lung cancer (NSCLC) patients, in a bid to provide a guidance for clinical treatment. Methods: Twenty-four cases of advanced NSCLC (stage III-IV) patients were treated with A regimen ...     

吉西他滨诱导胰腺癌细胞PANC-1中甲基化诱导静止基因的表达与半胱氨酸天冬氨酸酶-1、核转录因子活性的研究

目的检测吉西他滨（gemeitabine,GEM）诱导胰腺癌细胞株PANC-1中甲基化诱导静止基因（TMSl／ASC）的表达,并探讨半胱氨酸天冬氨酸酶-1（cysteine aspartase,caspase-1）、核转录因子（nuclear factor—κB,NF—κB）的活性与TMSl／ASC之间的关系。方法用噻唑蓝（methyl thiazolyl tetrazolium,MTr）比色法检测GEM在不同浓度（1、2、4、8、16μg／m1）及不同时间（24、48h）下对胰腺癌细胞PANC-1存活率的影响;RT—PCR技术检测PANC—1细胞在GEM（4．27μg／m1）刺激组（实验组）和空白组（对照组）培养24h和48h后TMS1／ASCmRNA的表达情况。用抗KB抑制蛋白（inhibitory protein of NF—κB,IKBR）多克隆抗体、抗caspase-1多克隆抗体和内参β—actin单克隆抗体通过Western blot技术检测并比较IKBa和caspase-1在实验组和对照组中的蛋白表达水平,从而分析NF．KB和caspase-1的活化状态。结果GEM对PANC-1细胞生长的抑制有浓度和时间依赖性,其半数抑制率（IC50）为24h4．27μg／ml;24h时实验组和对照组TMSl／ASC的表达量分别为（0．3±0．004）和（0．1±0．001）,48h实验组和对照组分别为（0．63±0．007）和（0．21±0．006）,2组相比较,差异有统计学意义（P〈0．01）。Westernblot结果显示：随着培养时间延长,caspase-1在对照组中未发生活化,GEM可促进其活化;GEM实验组与对照组相比It（Bet的表达量无明显变化,GEM不能促使NF—KB活化。结论GEM能抑制胰腺癌PANC-1细胞增殖并促进凋亡,随着作用时间的延长其药物敏感性减低。GEM作用-定时间可诱导TMS1／ASC表达增加,caspase-1可能参与GEM诱导胰腺癌细胞株PANC-1凋亡的信号转导途径,NF-κB不参与GEM诱导胰腺癌细胞株PANC—1凋亡的信号转导途径。     

吉西他滨联合长春瑞滨方案复治对紫杉醇联合顺铂方案疗效欠佳的晚期非小细胞肺癌24例临床观察

 目的 评价吉西他滨（GEM）联合长春瑞滨（NVB）方案复治对紫衫醇（TAX）联合顺铂（DDP）方案疗效欠佳的晚期非小细胞肺癌（NSCLC）的疗效、生存期及不良反应。方法 24例既往行TAX联合DDP治疗后疗效评价为稳定或进展的晚期NSCLC患者，继续用GEM联合NVB方案治疗，两周期后评价近期疗效和不良反应。结果 24例患者近期有效期29.2 ％，中位生存期28周，一年生存率34.3 %。结论 GEM联合NVB方案复治对TP方案疗效差的NSCLC患者有一定疗效，无交叉耐药性，可使患者病情进展延缓，中位生存期延长，且毒性可耐受。     

End-of-life care for older people in subacute care: A retrospective clinical audit

Background

With an ageing population and chronic illness the leading cause of death, challenges exist in meeting the healthcare needs of older people. For older people, care may be provided in subacute care services where, although the focus is on rehabilitation and optimisation of functioning, many older people will die.

Lactococcus lactis-based vaccines from laboratory bench to human use: an overview

Developing effective vaccines is an important weapon in the battle against potential pathogens and their evolving antibiotic resistance trends. Several vaccine delivery vectors have been investigated among which the generally regarded as safe (GRAS) Lactococcus lactis has a distinguished position. In this review, different factors affecting the efficacy of L. lactis-based vaccines are discussed. In addition, the issues of biological containment and pharmaceutical quality assurance of L. lactis vaccines are highlighted. These issues are critical for the success of medical translation of L. lactis-based vaccines from research laboratories to clinical use by ensuring consistent manufacturing of safe and efficacious vaccines.     

吉西他滨联合顺铂治疗晚期非小细胞肺癌的临床研究

目的 观察吉西他滨（gemcitabine，GEM）联合顺铂方案治疗晚期非小细胞肺癌的疗效及不良反应。方法 对经病理组织学或细胞学诊断证实的56例晚期非小细胞肺癌患者采用GP方案行静脉化疗：GEM1000mg／m^2，静脉滴注，d1，d8；DDP30mg／m^2，静脉滴注，d1～d3；21天重复，至少治疗2个周期。结果 可评价疗效56例，完全缓解（CR）5．3％（3／56），部分缓解（PR）42．9％（24／56），稳定（SD）33．9％（19／56），进展（PD）17．9％（10／56），总有效率（RR）48．2％（27／56）；肿瘤控制率（CR＋PR＋SD）为82．1％（46／56）；中位缓解期7．4个月，中位生存期11．3个月；不良反应以白细胞及血小板减少，消化道反应，乏力为常见，患者均可耐受，无化疗相关死亡。结论 吉西他滨联合顺铂对晚期非小细胞肺癌有较好疗效，不良反应可为患者所耐受，值得临床应用。     

吉西他滨对胰腺癌细胞PANC-1活性和蛋白表达的影响

目的：研究吉西他滨（健择,Gemcitabine,GEM）对胰腺癌细胞PANC-1活性及蛋白表达的影响。方法：应用噻唑蓝（MTT）比色法检测吉西他滨在不同时间（12h、24h、36h、48h）下对胰腺癌细胞PANC-1存活率的影响,透射电镜观察吉西他滨对胰腺癌细胞PANC-1形态的影响,蛋白印迹法观察经吉西他滨作用前后蛋白的表达。结果：吉西他滨对PANC-1细胞生长的抑制有时间依赖性,透射电镜观察胰腺癌细胞发生核质疏松,核膜分层、起泡甚至破裂,核质溢出,胞浆也出现空泡,细胞膜和细胞器发生明显改变,随而质膜渗透性增加并细胞溶解,蛋白印迹法显示,GEM影响蛋白质表达。结论：吉西他滨对胰腺癌细胞PANC-1的生长具有显著抑制作用。药物敏感性降低和作用时间延长能导致蛋白的表达及改变。     

PET imaging for attention deficit preclinical drug testing in neurofibromatosis-1 mice

Attention system abnormalities represent a significant barrier to scholastic achievement in children with neurofibromatosis-1 (NF1). Using a novel mouse model of NF1-associated attention deficit (ADD), we demonstrate a presynaptic defect in striatal dopaminergic homeostasis and leverage this finding to apply [¹¹C]-raclopride positron-emission tomography (PET) in the intact animal. While methylphenidate and l-Deprenyl correct both striatal dopamine levels on PET imaging and defective attention system function in Nf1 mutant mice, pharmacologic agents that target de-regulated cyclic AMP and RAS signaling in these mice do not. These studies establish a robust preclinical model to evaluate promising agents for NF1-associated ADD.