替莫唑胺联合伽马刀与单纯伽马刀治疗脑转移癌疗效比较

目的 分析比较替莫唑胺联合伽马刀治疗脑转移癌与单独伽马刀治疗脑转移癌的临床疗效以及不良反应.方法 将确诊脑转移癌病人34例,分成两组:单独伽马刀治疗组(单独组,总剂量35~48 Gy/10~12 f);替莫唑胺联合伽马刀治疗组(联合组,伽马刀治疗期间同时予以口服替莫唑胺150 mg·m-2·d-1,d1~5,放疗结束后继续予以3周期替莫唑胺辅助化疗,方案为150 mg·m-2·d-1,d1~5,28 d为1周期).比较分析两组近期疗效以及不良反应.结果 单独组和联合组治疗近期有效率分别为56.25%和88.89%(P=0.031),1年生存率分别为43.75%和55.56%(P=0.216).两组白细胞、血小板减少发生概率相似(P>0.05).急性脑损伤发生率较高,均以I级损伤为主(联合组为44.44%,单独组为50%).结论 替莫唑胺联合伽马刀治疗脑转移癌是一种安全有效的新型治疗手段,病人耐受性较好.     

正交试验法优选棘茎木皂苷提取工艺及抗炎镇痛作用的实验研究

目的利用正交试验法优选棘茎楤木皂苷提取工艺及抗炎镇痛作用药理实验。方法利用简便常用的正交试验设计优化棘茎楤木根皮总皂苷提取工艺,并采用二甲苯致小鼠耳肿胀、角叉菜胶致大鼠足肿胀、醋酸致小鼠扭体反应实验等急性炎症动物模型及疼痛模型,观察棘茎楤木皂苷的抗炎镇痛作用。结果正交试验优选出棘茎楤木皂苷提取工艺为:10倍量95%的乙醇回流提取3次,每次0.5h;药理实验初步表明棘茎楤木皂苷具有抗炎镇痛作用。结论棘茎楤木皂苷含量较高,可以开发成治疗风湿疾病的医药中间体。     

Effects of Intrathecal Injection of Nicotine on the Analgesic Effects of Isoflurane in a Model of Inflammatory Pain

Abstract: The present study was designed to investigate the role of spinal neuronal nicotinic acetylcholine receptors in the analgesic effects of isoflurane. After having established the mice model of analgesia by intraperitoneally injecting (i.p.) appropriate doses of isoflurane, nicotine, a neuronal nicotinic acetylcholine receptor agonist was intrathecally injected. The effects of isoflurane and nicotine on paw licking times and formalin‐induced c‐fos expression in the spinal cord dorsal horn were examined. Our correlative studies have shown that isoflurane can decrease the paw licking times and simultaneously suppress c‐fos expression after injection of formalin in the mice. Nicotine can partially antagonize the effects induced by isoflurane above. Spinal neuronal nicotinic acetylcholine receptors may be important targets for the analgesic effects of isoflurane in formalin pain.     

Biocompatibility assessment of nanomaterials for environmental safety screening

In view of the extensive use of nanoparticles in countless applications, a fast and effective method for assessing their potential adverse effects on the environment and human health is extremely important. At present, in vitro cell‐based assays are the standard approach for screening chemicals for cytotoxicity because of their relative simplicity, sensitivity, and cost‐effectiveness compared with animal studies. Regrettably, such cell‐based viability assays encounter limitations when applied to determining the biological toxicity of nanomaterials, which often interact with assay components and produce unreliable outcomes. We have established a cell‐impedance‐based, label‐free, real‐time cell‐monitoring platform suitable for use in a variety of mammalian cell lines that displays results as cell index values. In addition to this real‐time screening platform, other traditional cytotoxicity assays were employed to validate cytotoxicity assessments. We suggest that the cell impedance measurement approach is effective and better suited to determining the cytotoxicity of nanomaterials for environmental safety screening. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1170–1182, 2017.     

KTDA抑制肿瘤细胞增殖和诱导凋亡的研究

目的探讨3-Keto-tirucall-8,24-dien-21-oic acid(KTDA)体外抑制肿瘤细胞增殖及诱导凋亡的作用。方法使用四甲基偶氮唑蓝(MTT)法观察KTDA对肿瘤细胞的增殖抑制作用;通过吖啶橙染色,观察肿瘤细胞的形态学变化;琼脂糖凝胶电泳法检测它们对细胞DNA降解的影响。结果KTDA浓度为100、10、1μg.mL-1,作用72 h时,能抑制人乳腺癌细胞系MCF-7、人肝癌细胞株SMMC-7721、人慢性髓性白血病细胞系K562、人宫颈癌细胞系Hela、人舌癌细胞系Tca 8113的生长,并呈浓度依赖性。当KTDA浓度为10μg.mL-1时,处理72 h后,于荧光显微镜下观察到凋亡小体,电泳结果显示典型的DNA梯状条带。结论KTDA能抑制5种肿瘤细胞的增殖,并呈浓度依赖性,KTDA对MCF-7、SMMC-7721、K562、Hela比较敏感,Tca 8113次之,其机制可能为通过诱导5种肿瘤细胞凋亡而发挥抗肿瘤的作用。     

修正酸碱失衡预计代偿公式的初步研究

目的编制更为合理的单纯性酸碱失衡预计代偿范围计算公式。方法采纳Hamm公式的最大代偿系数及周寿生公式的代偿范围,编制成修正代偿公式。结果修正酸碱失衡预计代偿公式（修正公式）有A、B两种表达式,其最后计算结果完全一致,A表达式：代谢性酸中毒：PaCO2=40-1.4×△[HCO3-]↓＋（0-5）;代谢性碱中毒：PaCO2=40＋0.9×△[HCO3-]↑-（0-5）;急性呼吸性酸中毒：[HCO3-]=24＋0.175×△PaCO2↑-（0-3）;慢性呼吸性酸中毒：[HCO3-]=24＋0.55×△PaCO2↑-（0-3）;急性呼吸性碱中毒：[HCO3-]=24-0.25×△PaCO2↓＋（0-3）;慢性呼吸性碱中毒：[HCO3-]=24-0.5×△PaCO2↓＋（0-3）。B表达式与周寿生公式形式类似（略）。结论修正公式推理成立,无过度代偿,可减少双重性失衡的误判或漏判,且应用方便。     

舒肝解郁胶囊治疗消化道肿瘤伴发抑郁症的效果及患者GDNF表达

目的 研究舒肝解郁胶囊治疗消化道肿瘤伴发抑郁症状患者的疗效及血清GDNF的表达情况.方法 选取从2014年12月至2016年6月在本院接受治疗的消化道肿瘤患者88例为观察对象.按照数字法随机分为观察组与对照组各44例,患者均实施常规化疗治疗,对照组给予一般对症支持治疗,观察组则给予舒肝解郁胶囊,两组疗效比较.结果 观察组治疗总有效率为86.36％(38/44),显著高于对照组的68.18％(30/44);治疗后两组HAMD评分均显著低于治疗前且观察组低于对照组;治疗后两组GDNF水平均显著高于治疗前且观察组高于对照组;两组不良反应及死亡率比较,差异无统计学意义(P＞0.05).结论 舒肝解郁胶囊治疗消化道肿瘤伴发抑郁症状患者的疗效显著,可明显改善患者抑郁症状,具有一定安全性,而血清GDNF可能与患者抑郁程度存在密切相关.     

251例老年高血压患者血压昼夜节律异常分析

探讨老年高血压患者血压昼夜节律异常的特点。将老年高血压患者251例按年龄段分为老年1组(60～69岁,n=50)、老年2组(70～79岁,n=88)和老年3组(≥80岁,n=113),分析3组患者动态血压参数、动态血压昼夜节律异常发生率。3组患者动态血压参数,夜间平均收缩压(nSBP) 老年3组高于老年1组(P＜0.01),24 h平均舒张压(24hDBP)老年3组和老年2组均低于老年1组(P＜0.01),白天平均舒张压(dDBP)老年3组和老年2组均低于老年1组(P＜0.01和P＜0.05)。3组的血压昼夜节律异常率分别为78.00%、89.78%和92.04%。血压昼夜节律异常率老年3组显著高于老年1组(P＜0.05)。表明随增龄变化,老年高血压患者昼夜节律异常率增高。老年高血压患者血压昼夜节律异常多数表现为非杓型和反杓型血压,并随增龄变化老年高血压患者昼夜节律异常率增高。     

Role of 5-lipoxygenase pathway in the regulation of RAW 264.7 macrophage proliferation

Arachidonic acid (AA) metabolites control cell proliferation, among other physiologic functions. RAW 264.7 macrophages can metabolise AA through the cyclooxygenase and lipoxygenase (LOX) pathways. We aimed to study the role of AA-metabolites derived from 5-LOX in the control of RAW 264.7 macrophage growth. Our results show that zileuton, a specific 5-LOX inhibitor, and nordihydroguaiaretic acid (NDGA), a non-specific LOX inhibitor, inhibit cell proliferation and [(3)H]-thymidine incorporation in a concentration-dependent fashion. Growth inhibition induced by NDGA can be explained by an apoptotic process, while zileuton does not seem to induce apoptosis. Moreover, these treatments delay the cell cycle, as analysed by flow cytometry. On the other hand, the leukotriene (LT) B(4) receptor antagonist U-75302, the LTD(4) receptor antagonists LY-171883 and MK-571, and the cysteinyl-LT receptor antagonist REV-5901 also inhibit cell proliferation and [(3)H]-thymidine incorporation in a concentration-dependent manner, and delay the RAW 264.7 cell cycle. However, these antagonists did not induce annexin V staining, caspase activation or DNA fragmentation. Furthermore, we demonstrated that exogenous addition of LTB(4) or LTD(4) revert the cell growth inhibition induced by zileuton or the leukotriene receptor antagonists mentioned above. Finally, we observed that LTB(4) and LTD(4), in the absence of growth factors, have pro-proliferative effects on macrophages, and we obtained preliminary evidences that this effect could be through mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways. In conclusion, our results show that the interaction between LTB(4) and LTD(4) with its respective receptor is involved in the control of RAW 264.7 macrophage growth.