促进剂

Objective: To observe the motor function variation of focal cerebral ischemical reperfusion injury rats'limbs at different time. To observe the expression of PCNA and VEGF. To observe the effect to that index when electric acupuncture the"Quchi"and"Housanli". To observe the effect to the focal cerebral ischemical reperfusion injury rats, which are inject eNOS catastaltic, when electric acupuncture that two acupoints. Through observing of above all things , we study acupuncture's blood vessel regenerated effect to cerebral ischemia reperfusion injury region, approach the possibility of brain functional recovery angiogenesis which promoted by acupuncture, provide new consider and experiment accordings for deepening acupuncture therapy of the ischemia stroke.

研究目的：通过观察局灶性脑缺血再灌注损伤大鼠不同时间点肢体运动功能的变化及损伤脑组织核心增长蛋白、血管内皮细胞生长因子的表达情况，电针&曲池&、&后三里&穴对以上各指标的影响、电针&曲池&、&后三里&对给予eNOS抑制剂对局灶性脑缺血再灌注损伤大鼠的影响，研究针刺对大鼠脑缺血再灌注损伤区血管再生的作用，探讨针刺促进脑功能恢复的血管生成可能机制，为进一步深化针灸治疗缺血性中风的认识提供新的思路和实验依据。

Polarization measurements showed that HBPT can inhibit the anodic reactions of the copper in 0.5mol/L H2SO4 and accelerate the cathodal reactions and act as a kind of anodic inhibitor.

极化曲线研究表明3，5-二（2-吡啶基）－1，2，4-三唑在0.5mol/L硫酸溶液中对铜的阳极反应起抑制作用，对铜的阴极反应起促进作用，属於阳极型缓蚀剂。

In summary, the present study investigated the principle of WEH acting on the BDZ receptor and showed that this principle was not baicalin, wogonin, or chrysin.

Chrysin可作用在BDZ结合处，在小鼠大脑皮质之Ki值为75μM，并且依浓度的增加，对GABA促进氯离子通透量亦增加，显示其为BDZ之作用剂。

The patient of glucoside of strong to applying at the same time heart and diuretic should notice compensatory sylvite. 1.2 cause or aggravating infection candy is coriaceous of hormone fight phlogistic action, its are main the mechanism is to restrain inflammation to promote factor, restrain antigen antibody reaction, reduce blood capillary to connect appear a gender, reduce the toxin harm to airframe, relieve the symptom that inflammation reacts thereby.

对同时应用强心甙和利尿剂的患者应注重补充钾盐。1.2诱发或加重感染糖皮质激素的抗炎功能，其主要机制是抑制炎症促进因子、抑制抗原抗体反应、降低毛细血管通透性，减轻毒素对机体的损害，从而减轻炎症反应的症状。

Our experimentation demonstrates that dauricine inhidits platelet aggregation induced by the threshold concentration of adenosine diphosphate, arachidonic acid and collagen in the dose-dependent way in vitro in rabbits. The aggregatipn inhibition rates produced by dauri- cine 0.08 mg/ml for ADP, AA and Coll are 49.20%, 62.26% and 65.75% respectively.

结果表明，体内外给山豆根硷明显抑制ADP、AA和Coll诱导的血小板聚集，存在剂量依赖关系，在最大聚集率减少的同时：促进ADP、AA诱导的血小板聚集解聚，减慢Coll诱导血小板聚集速度；对三种促聚集剂的抑制无明显选择性。

It was found that the thermodynamically unfavourable isomerization of quadracyclane to norbornadiene could be accomplished in the presence of toluene or durene as a co-sensitizer.

首次发现在甲苯、杜苯等芳烃共敏化下，可以使原来不能进行的、热力学不利的四环烷→降冰片二烯异构化得以进行，并根据CIDNP结果提出这是由于生成了敏化剂/底物/芳烃三元基激络合物使反应的势能面改变造成的并促进单线态的系间窜跃。

AIM: To observe the effect of endothelin receptor antagonist (BQ123) on calcification in rat vascular smooth muscle cells in vitro. METHODS: Calcification of cultured rat VSMCs was produced by incubation with β-glycerophosphate.

目的：在离体钙化的血管平滑肌细胞上，观察内皮素受体阻断剂对血管平滑肌细胞钙化的影响，探讨内皮素促进细胞钙化的信号转导和分子机制。

METHODS:Calcification of cultured rat VSMCs was produced by incubation with β-glycerophosphate. Calcium content, Ca2+ deposition and alkaline phosphatase activity were analyzed to estimate the extent of calcification.

目的：在离体钙化的血管平滑肌细胞上，观察内皮素受体阻断剂对血管平滑肌细胞钙化的影响，探讨内皮素促进细胞钙化的信号转导和分子机制。

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。

Objective To study the permeation of meloxicam in rats with enhancer mentha oil and azone.

摘要目的考察薄荷油和azone 2种促渗剂对美洛昔康的渗透促进作用。

With Death guitarist Schuldiner adopting vocal duties, the band made a major impact on the scene.

随着死亡的吉他手Schuldiner接受主唱的职务，乐队在现实中树立了重要的影响。

But he could still end up breakfasting on Swiss-government issue muesli because all six are accused of nicking around 45 million pounds they should have paid to FIFA.

不过他最后仍有可能沦为瑞士政府&议事餐桌&上的一道早餐，因为这所有六个人都被指控把本应支付给国际足联的大约4500万英镑骗了个精光。