Anti-angiogenesis effect of generation 4 polyamidoamine/vascular endothelial growth factor antisense oligodeoxynucleotide on breast cancer in vitro

Objective: To study the effects of the generation 4 polyamidoamine/vascular endothelial growth factor antisense oligodeoxynucleotide (G4PAMAMNEGFASODN) compound on the expressions of vascular endothelial growth factor (VEGF) and its mRNA of breast cancer cells and on the inhibition of vascular endothelial cells. Methods: We examined the morphology of G4PAMAM/VEGFASODN compound and its pH stability, in vitro transfection efficiency and toxicity, and the expressions of VEGF and its mRNA. Methyl thiazolyl tetrazolium assay was used to detect the inhibitory function of the compound on vascular endothelial cells. Results: The compound was about 10 nm in diameter and was homogeneously netlike. From pH 5 to 10, it showed quite a buffered ability. The 48-h transfection rate in the charge ratio of 1:40 was 98.76%, significantly higher than that of the liposome group (P<0.05). None of the transfection products showed obvious toxicity on the cells. The expressions of both VEGF protein and its mRNA after G4PAMAM/VEGFASODN transfection decreased markedly. Conclusion: With a low toxicity, high safety, and high transfection rate, G4PAMAMNEGFASODN could be a promising gene vector. Specifically, it inhibits VEGF gene expression efficiently, laying a basis for further in vivo animal studies.     

过度运动对肾脏细胞外基质、金属蛋白酶及其抑制因子影响的实验研究

通过在不同运动负荷的运动训练状态下,观察大鼠肾脏组织Col IV、Laminin蛋白、MMP-9酶的表达和尿TP排泄率的变化,以及不同的运动负荷对MMP-9、TIMP-1和ColIVmRNA基因表达的影响,研究不同负荷的运动训练对大鼠肾脏ECM、MMP-9/TIMP-1的影响以及MMP-9/TIMP-1的变化在导致肾脏组织结构、生理功能损害上的作用,进一步探讨运动性蛋白尿的产生机制.实验结果表明:经过8周的过度训练后,C组大鼠肾脏Col IV、Laminin相对于A、B两组出现重度阳性表达,具有显著性差异:Col IV、MMP-9、TIMP-1mRNA表达显著增强,TIMP-1mRNA的表达上调了225%显著大于MMP-9mRNA表达上调147%.且尿TP排泄率也显著升高.说明过度运动训练导致ECM产生增加,降解能力下降,致使肾小球及肾小管基底膜ECM异常代谢、沉积和肾间质纤维化的发生和加剧,肾脏组织超微结构及生理功能受到损害.     

原电池教学设计

基础教育课程改革倡导师生在教学中进行科学探究，让学生自行建构知识网络。根据这种理念，就原电池一节的教学设计了一种科学探究的教学模式。     

纳米氧化镍在铁镍蓄电池中的应用研究

通过硝酸镍溶液和尿素溶液，采用均相沉淀法制备出纳米氧化镍，以纳米氧化镍取代传统的普通氧化镍和碳棒一起制成纳米氧化镍电极，应用于铁镍蓄电池中。研究了其电化学性能，比较了纳米氧化镍蓄电池和非纳米氧化镍蓄电池充放电特性，发现前者的放电性能明显优于后者，其充电性能也表现出更好的态势。     

不同强度力竭运动大鼠运动后12h肝细胞凋亡的研究

研究对象、方法:利用细胞免疫组化的方法研究力竭运动后12 h成年雄性SD大鼠肝细胞凋亡同肝细胞内的自由基水平和钙代谢之间的关系。结果:1)运动组与C组相比,凋亡细胞的数量差异显著(p<0.05);运动组组间差异也具有显著意义(p<0.05)。2)ME、HE组肝细胞内SOD活性与C组相比差异显著(p<0.05),但运动组组间差异不显著。3)ME组肝细胞中MDA含量增加、GSH含量降低,且相对于对照组差异显著(p<0.05);HE组虽有类似变化,但与其它各组相比无显著性差异。4)运动组肝细胞中Ca2+含量较对照组增加,差异显著(ME:p<0.01,HE:p<0.05),运动组组间差异显著(p<0.05)。结论:1)力竭运动可导致肝细胞凋亡,氧化应激及钙离子超载是引起细胞凋亡的重要因素,且前者可能发挥更重要作用。2)中等强度力竭运动更易于导致肝细胞凋亡,其原因可能同长时间力竭运动引起中暑或严重缺水,进而导致恢复期内中性粒细胞发生呼吸爆发有关。     

运动与Th细胞和ICOS分子研究新进展

最新研究表明,超量运动中Th2细胞因子IL-4、IL-6、IL-10及TNF-α水平的明显上调及应激激素的大量分泌,造成Th1和Th2之比失衡,进而导致体液免疫功能增强、细胞免疫功能相对低下,是继慢性运动后感染性疾病发病率增高的主要原因.而运动应激以及运动中损伤则是免疫系统应答的激活因子.诱导性协同刺激分子在运动后活化T细胞上的表达及其对Th2细胞的分化诱导,表明了它在运动免疫应答中重要而独特的作用.     

大鼠不同强度运动对肝细胞凋亡的影响

采用流式细胞术及原位缺口末端标记法(TUNEL),检测大鼠肝细胞凋亡;同时检测大鼠红细胞超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)的含量.结果发现,运动后肝细胞凋亡增加,且随着运动强度的加大,细胞凋亡百分率升高,反映机体抗氧化能力的SOD、GSH-Px显著降低,而MDA含量显著升高.认为,运动可诱导肝细胞凋亡,而运动后机体抗氧化能力下降,可能是凋亡发生的机制之一.     

Successful immunological treatment of gallbladder cancer in India―Case report

INTRODUCTION In cancer patients, tumor immunity is generally impaired. However, tumor immunity may occur in-vivo as circulating tumor-specific antibodies, with cytotoxic T lymphocytes (CTLs) having been identi- fied in cancer patients (Disis et al., 1997; Albert et al., 1998) suggesting that effective anti-tumor responses may be elicited through immunotherapeutic strategies. In recent years, a number of clinical trials have proved the safety and feasibility of using human dendritic cell…     

长期力竭性训练对大鼠海马神经元凋亡的影响

目的:研究长期力竭性训练对大鼠海马神经元凋亡的影响及其基因调控机制;方法:对大鼠进行为期8周的力竭性游泳训练,用DNA原位末端标记法检测海马神经元的凋亡,并用免疫组化的方法观察海马神经元中bcl-2、bax的免疫反应活性;结果:1)长期力竭性训练后,大鼠海马神经元凋亡显著增加.海马神经元凋亡可能是力竭性训练导致运动能力降低和中枢性运动疲劳的病理生理机制.2)长期力竭性训练后,大鼠海马神经元中bcl-2蛋白的表达显著下降,bax蛋白的表达显著增加.因此,力竭性训练可抑制海马神经元bcl-2蛋白的表达而促进bax蛋白的表达,这可能是力竭性训练导致大鼠海马神经元凋亡发生的基因调控机制.     

Resting MAPK expression in chronically trained endurance runners

Purpose: There is a paucity of research investigating the expression of mitogen-activated protein kinases (MAPK) in chronically trained (CT) athletes. Thus, it is unclear how MAPK may contribute to performance and muscle adaptation in CT subjects. The purpose of this study was to determine MAPK total protein, and phosphorylated expression of extracellular signal-regulated kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38-MAPK (p38) between untrained, and chronically trained runners. Methods: Tissue samples were analysed from sedentary (SED; n?=?5) controls and chronically trained runners (CT; n?=?5). Resting muscle biopsy samples were analysed for total-MAPK – and ratio of phosphorylated/total (p-MAPK) – ERK1/2, JNK, and p38-MAPK via western blotting. Mann–Whitney U tests and effect sizes were utilized to determine differences in total MAPK protein content and phosphorylation status between SED and CT subjects. Results: There was no difference in total-MAPK expression between SED and CT (p?>?.05). p-p38-MAPK tended to be greater for CT compared to SED (p?=?.07). There were moderate effect sizes of decreased pERK/total-ERK (d?=??0.69) and increased pJNK/total-JNK (d?=?0.54) in CT compared to SED. There was a positive correlation between p-p38-MAPK/total-MAPK and the percentage of type I fibres (r?=?0.73, p?=?.016). Conclusion: Contrary to previous studies, chronic endurance training does not greatly influence total MAPK protein expression in chronically trained runners. However, resting phosphorylation of p38-MAPK may contribute to enhanced oxidative metabolism at chronically trained levels. These alterations are likely involved in the different physiological adaptations that occur following long-term training or at highly competitive levels.