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It was concluded that PG not only played an important role in trimer formation but also effected the pigments binding and the energy transfer within the LHCⅡ.

以上实验结果证明,PG及其反式十六碳一烯酸不仅在LHCⅡ三聚体的形成中具重要作用,而且还影响色素分子在LHCⅡ三聚体中的结合状态以及叶绿素b到叶绿素a的正常能量传递。

The development speed of gynogenetic embryos was later than that of the control group, and aneuploids were found in this study. The obvious improved survival of trochophore larvae with a peak at 40s UV exposure suggested the presence of a Hertwig effect in the gynogenesis of A. pectinata. When sperms were irradiated for 40s, the cleavage rate was relatively high (51.2%), the developmental rate of D-larvae became zero, and the rate of haploid reached the highest (36.8%).

经紫外线照射的精子受精后所产生的单倍体胚胎发育速度慢于正常受精所产生的二倍体胚胎,各照射组均出现非整倍体。40s照射组中卵裂率达到51.2%,D型幼虫发生率为0,单倍体率最高,达到36.8%,出现"Hertwig效应"。

RESULTS: The mild traction group showed angulus anterior individual neuron slightly engorged, neuron and nerve fiber morphous was normal essentially; individual substantia alba demyelinates in fragmentis; medullary sheath and auxiliary fibers of nerve root were hydropsia slightly without conspicuous myelinolysis. The moderate traction group demonstrated myelinolysis change in the spinal cord, and neurofibras lined up chaos, auxiliary fibers disaggregated, neuron dropsy, tigroid body disappeared with karyopycnosis and anachromasis in neurons; nerve root showed myelinolysis. The severe traction group displayed a great demyelination region; anterior motor neurons with karyopycnosis and anachromasis; myelinated nerve fiber of nerve root shrinked, decreased in number, with severe demyelination changes.

结果:轻度牵拉组牵拉侧前角个别神经元稍肿胀,神经元及神经纤维形态基本上正常,个别白质小片状脱髓鞘样改变,神经根髓鞘和轴索轻度水肿,脱髓鞘不明显;中度牵拉组白质有脱髓鞘改变,神经纤维排列紊乱,轴索崩解、断裂;灰质神经元水肿明显加重,前角运动神经原细胞尼氏体消失,核固缩、深染,神经根髓鞘和轴索水肿,局部轻度脱髓鞘改变;重度牵拉组牵拉侧白质为不规则的大片脱髓鞘区,前角运动神经元胞体固缩、变形、核深染,神经根有髓神经纤维萎缩、数目减少,重度脱髓鞘改变。

The stem segments of Cerasus humilis Bunge with axillary bud were used as explant in this experiment and the natural regenaration plants were obtained in vitro culture of explants.

本试验以欧李当年生嫩枝上带有腋芽的茎段为外植体进行离体组织培养,获得了正常的再生植株。

This compressor but with dry device (adsorptive type, refrigerant type or draw type) form a complete set, make inside the dynamo outer circulation of hydric implementation airframe, ensure adsorptive type is dry the second birth of device is dry, although machine or turning condition stop to fall in the dynamo hydric still can be outside airframe is normal circulate, be worth in order to achieve the humidity inside the dynamo normally.

该缩小机可与躁热装置(附着式、冷藏式或者吸取式)匹配,使发电机内氢气完成体机外循环,保证附着式躁热装置的复生躁热,既便在发电机停机或者盘车态势下氢气仍可以在体机外正常循环,以达到和实现发电机内湿润程度正常值。

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示:1BP刺激细胞可促进c-Jun活化,并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性,均可明显抑制BP诱导的c-Jun活化,但阻断p38活性对BP引起的c-Jun活化无明显影响,提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化,并降低磷酸化ERK的表达水平,但对磷酸化JNK的表达水平无明显影响,说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加,并同时诱导Akt和ERK的磷酸化水平的升高,表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况,发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加,提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化,降低磷酸化Rb以及E2F1蛋白表达水平,表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高,可见c-Jun也参与调控BP诱导的p53/p21通路活化。

IGF-I in hepatic cirrhosis correlated with body fat mass、body fat rate、BMI、insulin and ISI. 4 Patients with liver cirrhosis often have all kinds of incretionary and metabolic abnormality, among which insulin resistance an

因此,瘦素参与了肝硬化时的营养不良。3 肝硬化患者与正常对照组IGF-I水平无显著性差异,但肝硬化IGF-I与体脂量、体脂率、体重指数、胰岛素、胰岛素敏感指数相关。4 肝硬化患者存在多种内分泌和代谢异常,尤其是存在胰岛素抵抗和生长激素抵抗,ghrelin、瘦素升高可能都与此有关。

Scanning electron microscopy showed that the spores were shrinking and collapsing, and the mycelium walls were ramified and nodulated under combined application of Na2SeO3 65.714mg/kg+LaCl3 53.002mg/kg. Furthermore the surface ornamentation of cystidia became fuzzy and disappearing, and some cystidia were disappearing and collapsing.

扫描电镜观察结果表明,与对照相比,中浓度硒镧配施(Na2SeO3 65.714mg/kg + LaCl3 53.002mg/kg)时,孢子由正常椭圆形变成全部萎缩,菌丝粗壮;囊状体在较低硒镧配施浓度(Na2SeO3 43.810mg/kg + LaCl3 35.335mg/kg)处理时表面纹饰模糊、消失,个别囊状体破裂,表面带有藤蔓状的组织。

After the cell growth curves was recorded, RPE cells of the 3-5th passages were utilized. 2、Three different siRNA (siRNAl,siRNA2,siRNA3) targeting against human cx43 gene and one negative control siRNA were designed and transfected into cultured human RPE cells via liposome reagent. The most effective siRNA can be determined by semi-quantitative reverse transcription PCRRT-PCR. 3、To the most effective siRNA, after transfected into human RPEs with different concentration, the cellular proliferate activities were messured by MTT colorimetry ; the percentages of RPE in different cell circle phase was assayed by FCM; the changes of phenotypical properities were observed with SCM; the protein expression of cx43 was studied through immunocytochemistry stain and Weston blot; the communication intercellular was calculated with FRAP; and the ability of recovery was assessed by using an in vitro wound healing model.4、The total proteins of siRNA1 and RPE were seperated by two-dimensional gel electrophoresis and visualized by silver staining. Proteins with significant expression alterations were selected and their peptide mass fingerprints (PMFs were obtained by matrix-assisted laser desorption/ionization time of flying mass spectrometry (MALDI-TOF-MS).The PMFs were used to search NCBInr database by Auto MS-Fit software.

实验方法:1、培养原代的人RPE细胞,经过细胞角蛋白、S-100和神经胶质原纤维酸性蛋白免疫细胞化学鉴定后,通过AO/PI染色技术确定培养细胞的存活率,描记其生长曲线,第3-5代用于以下细胞实验2、生物合成针对人cx43基因的三条小干扰RNA和一条阴性RNA通过脂质体转染RPE细胞后,通过RT-PCR的方法确定抑制效率最高的干扰片断3、将该片段以不同浓度通过阳离子脂质体转染培养的人RPE细胞后,采用MTT法观察其对细胞的增殖力的作用;通过流式细胞仪观察其对细胞周期的影响;通过扫描电镜观察其对细胞形态的影响;通过免疫细胞化学和Weston blot观察其对cx43蛋白表达的作用;采用激光共聚焦和荧光淬灭恢复技术观察荧光恢复速率平均百分率,评价其对细胞间通讯功能的影响;通过制作RPE细胞损伤模型,观察其对损伤修复能力的作用4、分离纯化转染siRNA的RPE组和正常对照组RPE细胞的全部蛋白质,应用等电聚焦电泳和SDS-PAGE双向电泳技术,银染显示分离出的蛋白质斑点,经凝胶图像分析软件对两个样本进行胶图分析,寻找差异蛋白点。

Signalling through CXCR4 mediates actin polymerization and pseudopodia formation in cells, and induces chemotactic and migration to target organs. In addition, CXCR4-SDF-1 axis can promote tumor angiogenesis and growth.

CXCR4在肿瘤组织中的表达明显高于正常组织,而肿瘤常见转移部位均为CXCR4的配体基质细胞衍生因子-1(stromal cell derived factor-1,SDF-1)表达丰富的器官,SDF-1与CXCR4结合后可使细胞肌动蛋白丝聚合,形成伪足,从而定向诱导肿瘤细胞迁移到特定的靶器官;此外,CXCR4与其配体SDF-1相互作用可以促进局部新生血管作用,利于肿瘤生长。

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