被抑制

The group disposed by Acetylspiramycin doesn"t show parallel results; The strip gray scale of exotoxin A decreased gradually with the increasing dosages of Azithromycin and Roxithromycin, which doesn"t show in group disposed by Acetylspiramycin and group PAO-JP2; The strip gray scale of lasR, detected by RT-PCR, decreased gradually with the increasing dosages of Azithromycin, which doesnt show in group PAO-JP2.Conclusions: There were obvious differences between PAO1 and PAO-JP2 in biology characteristics in vitro.

本研究发现大环内酯类药物在生物被膜培养过程中分别处理PAO1、PAO-JP2，结果提示大环内酯类药物(14、15元环)通过对QS系统的影响可有效抑制铜绿假单胞菌生物被膜的形成；通过QS系统有效抑制铜绿假单胞菌的毒力因子的产生，16元环的大环内酯类药物乙酰螺旋霉未见上述结论；lasR基因的反转录结果提示阿奇霉素可在转录水平抑制QS系统发挥其作用。

The extent of inhibition of depolarization by superfusion of ethanol for 5 minutes was 41.8±3.3 ％(n=17). The addition of 5 nM and 20 nM KT5720 (a selective protein kinase A inhibitor) and 250 μM H9 dihydrochloride (a non-selective protein kinase inhibitor), into the intracellular solution significantly attenuated the inhibitory effects of ethanol.

当分别将5 nM或20 nM KT5720（选择性蛋白质激酶A抑制剂）或250 μM H9 dihydrochoride（非选择性蛋白质激酶抑制剂）置入细胞内液时，乙醇的抑制作用明显被减弱；但乙醇的抑制作用不受到5 nM或20 nM calyculin A（磷酸酶1/2A抑制剂）的影响。

For most viruses,there is aneed for antimicrobials that target unique viral molecular properties.Acycloviris one such drug.It is activated into ahuman herpesvirusDNA polymerase inhibitor exclusively by HHV kinases and,thus,does not suppress other viruses.Here,we show that ACV suppresses HIV-1in HHV-coinfected human tissues,but not in HHV-free tissue or cell cultures.However,addition of HHV-6-infected cells renders these cultures sensitive to anti-HIV ACV activity.We hypothesized that such HIV suppression requires ACV phosphorylation by HHV kinases.Indeed,an ACV monophosphorylated prodrug bypasses the HHV requirement for HIV suppression.Furthermore,phosphorylated ACV directly inhibits HIV-1reverse transcriptase,terminating DNA chain elongation,and can trap RT at the termination site.These data suggest that ACV anti-HIV-1activity may contribute to the response of HIV/HHV-coinfected patients to ACV treatment and could guide strategies for the development of new HIV-1RT inhibitors.

对大多数病毒而言，都需要有针对其分子特性的靶向杀毒剂阿昔洛韦就是这样一种靶向药物在人疱疹病毒酶的特定作用下，阿昔洛韦被激活成为人疱疹病毒DNA聚合酶抑制剂，因此不能再抑制其它的病毒我们的研究发现阿昔洛韦在共感染人疱疹病毒的组织中可以抑制HIV-1，但在无人疱疹病毒感染的组织或细胞中无此作用然而，加入人疱疹病毒-6感染的细胞却使得其对抗HIV的阿昔洛韦变得敏感我们推测这种抑制作用依赖于人疱疹病毒酶导致的阿昔洛韦磷酸化实际上，单磷酸化的阿昔洛韦前体药物无需人疱疹病毒的参与即可抑制HIV此外，磷酸化的阿昔洛韦能直接抑制HIV-1逆转录酶，将其阻止在终止位点，从而终止DNA链的延长这些结果提示阿昔洛韦的抗HIV-1活性决定了艾滋病病毒/人疱疹病毒共感染的患者对阿昔洛韦的治疗反应，也有助于开发新的HIV-1逆转录酶抑制剂

This subset is hyporesponsive and anergic to antigen stimulation. Recently, it has been demonstrated to participate in the immune deficiency in human immunodeficiency virus infection and has close relationship with the development of acquired immunodeficiency syndrome. Meanwhile, the CD4(superscript +)D25(superscript +)Treg is also infected when the human body is invaded by HIV. The CD4(superscript +)CD25(superscript +)Treg will finally be killed by the mechanism of antibody-dependent cell-mediated cytotoxicity. Because of the decrease of the CD4(superscript +)CD25(superscript +)Treg, it can't function as a immune suppressor as a result of the excess of activation of HIV and gradually exhausting of the T cell, which shows that the CD4(superscript +)CD25(superscript +)Treg plays a inhibitory role in the different stages of the development of the HIV as well as different effects in the pathogenesis of AIDS.

它能够抑制自身免疫病的发生和发展，参与肿瘤免疫的调节，同时在感染和移植免疫中也发挥着极其重要的作用。T细胞的这一亚群具有免疫调节和免疫抑制的特性，新近发现它亦与爱滋病的发生、发展关系密切HIV进入人体后，CD4D25调节性T细胞抑制了机体的免疫效应但它也同时被感染，最终由于细胞毒的作用而死亡由于调节性T细胞数量的减少不能有效的发挥其抑制作用，HIV持续的过度活化使得T细胞逐渐耗竭说明在HIV发生、发展的不同阶段Treg细胞可能都发挥了免疫抑制作用，但是却对HIV感染与爱滋病发病的进程产生了不同的效应。

We show that, in primary breast tumour cells, this event causes decreased p53 levels and increased chemoresistance.

现在， NUMB 已被发现通过抑制泛素连接酶 Hdm2、从而防止主要肿瘤抑制因子 p53被破坏来起一种肿瘤抑制因子的作用。

In our system, we were unable to detect the cleavage product of overexpressed slit2. Nevertheless, it is interesting to investigate whether the cleavage of slit2 is important for its responsible function in CL1-5 or not. Our result showed that a non-cleavable slit2 showed similar growth inhibitory ability as the cleavable slit2. Therefore, the growth inhibitory ability of slit2 does not require cleavage at the reported cleavage site.

结果显示，在CL1-5细胞中，我们没有侦测到Slit2被切割的情形，并且当不能被切割的Slit2蛋白表现在CL1-5时，其抑制生长的能力与可被切割的Slit2相同，因此这个报导中的切割点与Slit2抑制生长的功能无关，而单独过度表现Slit2-C terminal蛋白片段就具有抑制细胞生长的能力。

The effect of genistein (0.8 mg/kg) was partially inhibited by L-NAME, or by sodium orthovanadate (50 μg/kg), a potent inhibitor of protein tyrosine phosphatase;(2) geni...

GST的这一效应可被L 硝基精氨酸甲酯部分阻断，预先注射蛋白酪氨酸磷酸酶抑制剂正钒酸钠( 5 0 μg/kg)，可部分抑制GST( 0 8mg/kg)引起的效应；( 2 )向肾血管灌注环路中直接注射GST也可剂量依赖性地降低肾动脉的灌流压，预先注射正钒酸钠可完全抑制GST引起的效应，而L NAME对此效应没有影响；( 3 )肠系膜血管灌流环路中注射GST可剂量依赖性地降低其灌流压，这一效应可被正钒酸钠部分抑制，而L NAME对此无影响。

The effect of genistein (0.8 mg/kg) was partially inhibited by L-NAME, or by sodium orthovanadate (50 μg/kg), a potent inhibitor of protein tyrosine phosphatase;(2) genistein also decreased the PP of renal vascular bed in a dose-dependent manner and the effect of genistein was completely inhibited by pretreatment with sodium orthovanadate, but unaffected by L-NAME; and (3) genistein decreased the PP of mesenteric vascular bed in a dose-dependent manner, an effect which was partially inhibited by sodium orthovanadate, but unaffected by L-NAME.

GST的这一效应可被L-硝基精氨酸甲酯部分阻断，预先注射蛋白酪氨酸磷酸酶抑制剂正钒酸钠(50 μg/kg)，可部分抑制GST (0.8 mg/kg)引起的效应；(2)向肾血管灌注环路中直接注射 GST 也可剂量依赖性地降低肾动脉的灌流压，预先注射正钒酸钠可完全抑制GST引起的效应，而L-NAME对此效应没有影响；(3)肠系膜血管灌流环路中注射GST可剂量依赖性地降低其灌流压，这一效应可被正钒酸钠部分抑制，而L-NAME对此无影响。

The effect of genistein (0.8 mg/kg) was partially inhibited by L-NAME, or by sodium orthovanadate (50 μg/kg), a potent inhibitor of protein tyrosine phosphatase;(2) Genistein also decreased the PP of renal vascular bed in a dose-dependent manner. The effect of genistein was completely inhibited by pretreatment with sodium orthovanadate, but unaffected by L-NAME;(3) Genistein decreased the PP of mesenteric vascular bed in a dose-dependent manner, an effect which was partially inhibited by sodium orthovanadate, but unaffected by L-NAME.

GST的这一效应可被L-硝基精氨酸甲酯部分阻断，预先注射蛋白酪氨酸磷酸酶抑制剂正钒酸钠(50 μg/kg)，可部分抑制GST (0.8 mg/kg)引起的效应；(2)向肾血管灌注环路中直接注射 GST 也可剂量依赖性地降低肾动脉的灌流压，预先注射正钒酸钠可完全抑制GST引起的效应，而L-NAME对此效应没有影响；(3)肠系膜血管灌流环路中注射GST可剂量依赖性地降低其灌流压，这一效应可被正钒酸钠部分抑制，而L-NAME对此无影响。

RESULTS:(1) ET-1 could increase total protein production, surface area, ERKs activity and ［Ca2+］i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.（2）The activation of ERKs and the increase of ［Ca2+］i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response.(3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of ［Ca2+］i, but not affect the activation of ERKs.

结果： ①ET-1浓度依赖性增加新生大鼠心肌细胞蛋白质含量和心肌细胞表面积、ERKs活性及［Ca2+］i浓度，以上作用可被ETA受体拮抗剂BQ123所完全抑制，被百日咳毒素部分抑制，而ETB受体拮抗剂BQ788则无效；②ERKs激酶特异性抑制剂PD98059可完全抑制ET-1激活ERKs的作用，钙通道拮抗剂硝苯地平可明显抑制ET-1介导的［Ca2+］i浓度增加，但二者皆仅部分抑制ET-1介导的心肌细胞肥大反应；③蛋白激酶C选择性抑制剂staurosporine并不能明显抑制ET-1介导的ERKs激活，但可抑制ET-1介导的的［Ca2+］i浓度增加及心肌细胞肥大反应。

On the other hand, the more important thing is because the urban housing is a kind of heterogeneity products.

另一方面，更重要的是由于城市住房是一种异质性产品。

Climate histogram is the fall that collects place measure calm value, cent serves as cross axle for a few equal interval, the area that the frequency that the value appears according to place is accumulated and becomes will be determined inside each interval, discharge the graph that rise with post, also be called histogram.

气候直方图是将所收集的降水量测定值，分为几个相等的区间作为横轴，并将各区间内所测定值依所出现的次数累积而成的面积，用柱子排起来的图形，也叫做柱状图。