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31.
携带小鼠白细胞介素-12基因的增殖型腺病毒对胃癌细胞的作用 总被引:5,自引:2,他引:3
目的观察携带小鼠白细胞介素12(mIL12)基因的增殖型腺病毒载体对胃癌细胞的杀伤作用及mIL12表达情况。方法以携带目的基因的增殖型腺病毒CNHK200mIL12感染人胃癌细胞株SGC7901、人正常肝细胞株L02。首先,通过荧光显微镜下观察、细胞杀伤实验等观察病毒对细胞的杀伤能力;其次,通过Westernblot分析及双抗体夹心法(ELISA)检测mIL12表达情况。结果CNHK200mIL12感染SGC7901后,当MOI=10时即可杀伤大部分的肿瘤细胞,与ONYX015相当,而对正常细胞无明显杀伤。ELISA检测表明mIL12基因表达量达(267.2±34.6)ng/5×105个细胞/48h,较复制缺陷型腺病毒载体高近百倍。结论CNHK200mIL12能在胃癌细胞中复制及增殖杀死胃癌细胞,并高水平表达目的基因。 相似文献
32.
Xinyu D. Li Esperanza Arias Ramamohana R. Jonnala Shyamala Mruthinti Jerry J. Buccafusco 《Journal of molecular neuroscience : MN》1996,27(3):325-336
The ability of nicotine to induce a cytoprotective or neuroprotective action occurs through several down-stream mechanisms.
One possibility is that the drug increases the expression of tyrosine kinase A (TrkA) nerve growth factor (NGF) receptors.
Certain β-amyloid peptides (e.g., Aβ1–42) have been shown to bind with high affinity to α7 nicotinic receptors and thus interfere
with a potentially neurotrophic influence. Treatment of differentiated PC-12 cells with nicotine produced a concentration-dependent
increase in cell-surface TrkA receptors that occurred concomitantly with cytoprotection. The effect of nicotine was blocked
by either of the α7 receptor antagonists α-bungarotoxin (α-BTX) or methyllycaconatine. The cytoprotective action of nicotine
also was inhibited by pretreatment with 10–100 nM Aβ1–42. Nicotine also was administered (four injections of 30 μg, spaced evenly over 24 h) to rats by direct injection into
a lateral cerebral ventricle. Brain TrkA expression was increased significantly in hippocampus and entorhinal cortex (up to
32% above control), with no changes found in cerebral cortex or hypothalamus. The nicotine-induced increases in TrKA expression
in hippocampus and entorhinal cortex were significantly inhibited by 10 μg α-BTX or by 10 nmol Aβ1–42. Therefore, physiologically
relevant concentrations of Aβ1–42 can prevent nicotine-induced TrkA receptor expression in brain regions containing cholinergic
neurons susceptible to the neurotoxicity associated with Alzheimer’s disease. 相似文献
33.
34.
The growth and development of vegan children 总被引:1,自引:0,他引:1
The results of prospective study on the growth and diets, estimated from 7-day weighed food intake records, of 20 life vegan children (aged 5.8–12.8 years) are presented. The growth and development of the children were normal but they tended to be lighter in weight and exceptionally lean compared with standards. Heights were around the median of the Tanner-Whitehouse standards but were lower than the medians recently proposed by the Department of Health. Energy intakes were similar to those reported in children of the same age in the general population, but dietary fibre intakes were very high which may have influenced the digestible energy. Sugar provided an average 15.6% of the dietary energy and this was supplied mainly by fruit and fruit juice. Mean fat intakes were close to the dietary reference values. Daily intakes of essential nutrients generally met the amounts recommended, with the exceptions of calcium and vitamin B12 . Many children received supplementary sources of vitamin B12 and only two children had intakes below the lower recommended nutrient intake. Intakes of saturated fatty acids were low and those of linoleic acid were high. The ratio of linoleic/α-linolenic acid was high. As docosahexaenoic acid is absent from vegan diets, it is suggested that vegans should use oils with a lower ratio of linoleic/α-linolenic acid. Future studies should also consider the influence of a vegan diet on retinal function. None of the children was immunized against whooping cough and 11 had not been immunized against polio: 16 of the children had suffered from whooping cough. Future studies need to take into account factors other than diet when assessing the health of vegans. The results of this study show that children can be successfully reared on a vegan diet providing sufficient care is taken to avoid the known pitfalls of a bulky diet and vitamin B12 deficiency. 相似文献
35.
Atsutoshi Ina Ken-Ichiro Hayashi Hiroshi Nozaki Yuto Kamei 《International journal of developmental neuroscience》2007,25(1):63-68
We identified and characterized a neurodifferentiation compound from the marine brown alga Sargassum fulvellum collected from the Japanese coastline. Several instrumental analyses revealed the compound to be pheophytin a. Pheophytin a did not itself promote neurite outgrowth of PC12 cells. However, when PC12 cells were treated with a low concentration of pheophytin a (3.9 microg/ml) in the presence of a low level of nerve growth factor (10 ng/ml), the compound produced neurite outgrowth similar to that produced by a high level of nerve growth factor (50 ng/ml). Pheophytin a also enhanced signal transduction in the mitogen-activated protein kinase signaling pathway, which is also induced by nerve growth factor. The effect of pheophytin a on neurite outgrowth of PC12 cells was completely blocked by U0126, a representative mitogen-activated protein kinase kinase inhibitor. These results suggest that pheophytin a enhances the neurodifferentiation of PC12 cells in the presence of a low level of nerve growth factor and that this effect is mediated by activation of a mitogen-activated protein kinase signaling pathway. 相似文献
36.
C. Hubeau M. Singer M. Lagranderie‡ G. Marchal† B. Vargaftig 《Clinical and experimental allergy》2003,33(3):386-393
37.
冠心病患者血清同型半胱氨酸与叶酸、维生素B12水平的变化 总被引:6,自引:0,他引:6
目的 探讨冠心病患者血清同型半胱氨酸(HCY)与叶酸、维生素B12浓度的变化及其相关性。方法 选择84例经冠状动脉造影术证实为冠心病的患者,应用荧光偏振免疫分析法(FPIA)测定血清HCY浓度,离子捕获免疫分析法(ICIA)测定血清叶酸浓度,非均相微粒子酶免疫分析法(MEIA)测定血清维生素B12浓度。结果 冠心病患者血清HCY浓度增高,与正常对照组比较有显著性意义(P<0.001),而叶酸、维生素B12浓度则降低,与正常对照组比较有显著性意义(P<0.001),以上两种变化呈负相关(P<0.001)。结论 同型半胱氨酸血症是冠心病的新的独立危险因素,叶酸、维生素B12缺乏可能是诱发高HCY的重要因素。 相似文献
38.
支气管哮喘是由Th2介导的Ⅰ型变态反应,与内源性IL-12生成不足有关,该文综述了IL-12的生物学效应、IL-12表达障碍与支气管哮喘的关系以及IL-12、重组IL-12(rIL-12)在支气管哮喘治疗方面的应用前景。IL-12与Ⅰ型变态反应关系密切,内源性IL-12表达不足使支气管哮喘患者免疫系统向Th2方向偏移,在过敏原或病毒等外因的刺激下发生支气管哮喘。用IL-12对支气管哮喘进行免疫治疗已在动物实验中取得了显著效果,将IL-12、rIL-12或IL-12的内源性诱生物应用于人体的方法也在不断探索中并取得了一定效果,基于IL-12的治疗方法可能为支气管哮喘等变应性疾病的免疫治疗开辟新的途径。 相似文献
39.
40.
利多卡因对N-甲基-D-天冬氨酸抑制大鼠肾上腺嗜铬细胞瘤细胞增殖的影响 总被引:2,自引:0,他引:2
目的 观察利多卡因对 N-甲基-D-天冬氨酸(NMDA)抑制大鼠肾上腺嗜铬细胞瘤细胞(PC12细胞)增殖的影响。方法 将体外培养的 PC12细胞分为6组,分别采用正常不含药液的培养基(C组);含400μmol·L(-1)NMDA 的培养基(N组);NMDA 分别混合10μmol·L~(-1)(L_1组)、10~2μmol·L~(-1)(L_2组)、10~3μmol·L~(-1)(L_3组)以及10~4μmol·L~(-1)(L_4组)利多卡因的培养基培养5d,应用流式细胞仪测定细胞 DNA 相对含量,解析细胞周期,计算 S 期细胞荧光强度占受测细胞总荧光强度的百分数为 S期分数(SPF)和 S 期与 G_2期细胞荧光强度之和与 M 期细胞荧光强度的比值[(S G_2)/M]。结果 与C 组比较,N、L_1组 SPF 和(S G_2)/M 均降低(P<0.05),L_4组 SPF 降低(P<0.05),而 L_2及 L_3组 SPF和(S G_2)/M 差异无统计学意义(P>0.05)。与 N 组比较,L_2、L_3及 L_4组 SPF 和(S G_2)/M 升高(P<0.05),L_1组 SPF 升高(P<0.05),而(S G_2)/M 差异无统计学意义(P>0.05)。结论 NMDA 可以通过抑制 PC12细胞 DNA 合成而影响细胞的增殖活性,利多卡因能拮抗 NMDA 对 PC12细胞增殖的抑制作用。 相似文献