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刺激-反应

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Because shave,stimulate wool bursa directly from time to tome, those who pass for many times is exciting, wool bursa can greaten , the beard that grows also can be jumped over thick, blacker, harder.

因为刮胡子时有直接的刺激到毛囊,经过多次的刺激,毛囊就会变大,长出来的胡须也就会越粗,越黑,越硬。

Objective: To investigate the visual attention mechanisms of brain through ERP technique by using the "cue-target" experimental paradigm, and the attended range were cued by different Chinese characters cue or region cue; the visual attention mechanisms of brain were investigated through ERP technique. Method:16 healthy young participants were involved. The stimulus trail included "background-cue-target". The background was comprised of three homocentric white circles.

目的:采用&提示-目标&的视觉实验范式,分别以汉字和范围提示不同等级的搜索范围,通过事件相关电位技术,研究视觉注意脑机制:方法:16名在校大学生作为有偿被试,刺激序列为背景-提示-靶刺激:背景由三个同心白色圆形线条组成。

The Second Affiliated Hospital, Medical School of Xian Jiaotong University, Xian 710004, ChinaABSTRACT: Objective To observe the acute homodynamic changes of biventricular pacing in patients with sick sinus syndrome and investigate the Ca2+ changes during absolute refractory period electrical stimulation by applying computer simulation.

目的 观察双心室起搏对病态窦房结综合征(sick sinus syndrome, SSS)患者的急性血液动力学变化及心脏绝对不应期电刺激对心功能的影响,通过计算机仿真研究,探讨绝对不应期电刺激的离子流作用机制。

Methods Granulocyte/macrophage colony stimulating factors and interleukin 4 were used to cultivate DC from peripheral blood of hepatocellular carcinoma patients.Tumor associated antigen extracted from human liver cancer HepG2 cell line was used to activate the DC,which will initiate homogenic T lymphocyte to form cytotoxic T lymphocyte.HepG2 cells were transplanted to the nude mice and were treated with CTL.Expression of PCNA in tumor cells was evaluated.

联合应用粒/巨细胞集落刺激因子及白介素-4(IL-4)直接从肝癌患者外周血中培养出DC;以源于人肝癌细胞系HepG2细胞的肿瘤抗原粗提物刺激DC;DC激活同源的T淋巴细胞产生细胞毒性T淋巴细胞;建立人肝癌细胞系HepG2裸鼠移植瘤模型;CTL治疗人肝癌细胞系HepG2裸鼠移植瘤;检测移植瘤标本肿瘤细胞PCNA表达水平。

Capsaicin excites nociceptive afferent nerves to produce warmth when initially applied, but with repeated application it desensitizes unmyelinated nerve fibers to produce hypalgesia without also causing patients to experience a reddening or blistering.

最初辣椒素刺激疼痛传入神经产生温暖,但通过它的反复刺激,使无髓神经纤维不敏感,从而产生痛觉迟钝,也没有造成患者能够体验到发红或者起泡。

2TNF-α in the concentration of 10-3-10u/ml significantly inhibited TSH-induced cAMP release by both normal and hyperfunctioning thyroid cells.

2在10~(-3)~10U/ml的浓度区间,TNF-α显著抑制TSH对正常和甲亢甲状腺细胞生成cAMP的刺激效应,10~3U/ml的TNF-α仅抑制TSH对正常甲状腺细胞的刺激作用,对甲亢甲状腺细胞无明显影响。

BMSCs and recombinant human GSF (50 μg/kg) were injected into models by tail vein and hypodermoclysis infusion respectively in the combination treatment group. Recombinant human GSF (50 μg/kg) was subcutaneously injected into models in the bone marrow stem cell autologous mobilization group. BMSCs were injected into rat models by tail vein in the BMSC group. Rat models in the heart failure group were intact.

造模后随机分成4组:联合治疗组尾静脉注射骨髓间充质细胞和皮下注入重组人粒细胞刺激因子50 μg/kg,自体骨髓干细胞动员组皮下注入重组人粒细胞刺激因子50 μg/kg,骨髓间充质干细胞组为尾静脉注射骨髓间充质细胞,心力衰竭组不给予任何干预。

Mid-pregnancy treatment of uterine fibroids:① myoma less than six centimeters in diameter, and asymptomatic, and regular prenatal checkups, the vast majority do not need special treatment;② leiomyoma diameter greater than 6 centimeters, with the the growth of uterine fibroids may continue to increase, while the large red-like leiomyoma easy change for the sake of stimulating the uterus to contract or peritoneal irritation, obstetricians refer only recommended in patients with bed rest and application of analgesic agent to conservative treatment, it is less recommended during pregnancy line hysteromyomectomy surgery, only as a last resort circumstances do myomectomy.

妊娠中期子宫肌瘤的处理:①肌瘤直径小于6厘米,且无症状者,定期产前检查,绝大多数不需特殊处理;②肌瘤直径大于6厘米,随着子宫的增长肌瘤还可能继续增大,而大型肌瘤易有红色样变而刺激子宫收缩或有腹膜刺激症状,介时产科医生只是建议患者卧床休息及应用止痛剂等进行保守治疗,很少建议在妊娠期行子宫肌瘤剔除手术,只有在不得已情况下才行肌瘤剔除术。

In training the computer system provided sequential stimulation to three key muscles groups(iliacus, quadriceps, shank triceps), In 3 cases with different level of spinal cord injury, the clinical application and curative effects were observed with this system.

锻炼每周进行3次,每次踏车10min,锻炼过程中,电脑控制多通道电刺激器在不同象限内顺序刺激双下肢的骼肌、股四头肌、小腿三头肌来完成踏车运动。在锻炼中记录自行踏车时间,并观察血压、脉搏的动态变化。

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。

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