抑制...

They were reversible un-competitive inhibitors, and their inhibition constants of free enzymeK(subscript I were 254.00 and 136.78 mmolL^(-1), respectively. Urea was reversible mixed-type inhibitor, and its inhibition constants of free enzymeK(subscript I and enzyme-substrate complexK(subscript IS were determined to be 379.02 and 1182.00 mmolL^(-1), respectively.

Na2SO3和H2O2对酶的抑制均表现为可逆反竞争性类型，它们对游离酶的抑制常数K(下标 I分别为254.00和136.78 mmolL^(-1)；尿素对酶的抑制表现为可逆的混合型抑制，它对游离酶的K和对酶－底物复合物的抑制常数K(下标 IS分别为379.02和1182.00 mmolL^(-1)。

The degradating and redistributing of ECM were migration of VSMC and vascular remodeling through inhibiting the production of PDGF-BB and the activation of MMPs so to prevent the vascular stenosis.⑤Orthotopic hybridism in situ: The expression of MMP-3 increased after operation, the tendency and intensity were parallel to the expression of NF-κB. Tongxinluo could decrease the expression of MMP-3 and NF-κB. The study showed that the producting and activating of MMP-3 were modulated by NF-κB. The inhibition to the producting and activating of MMp-3 of Tongxinluo was mediated by inhibiting the activating of NF-κB. Conclusion ①The rabbit vascular stenosis model could be established successfully by plain balloon damage, the operation process was easy, economical and practical.

①单纯球囊损伤可成功建立典型家兔血管狭窄模型，操作方法简单，经济实用；②以VSMC增殖、迁移为主的内膜增厚以及以ECM降解、合成与再分布所致的血管重构是导致受损血管狭窄的根本原因；③通心络能明显抑制VSMC的增殖、迁移和ECM降解、合成，阻止血管内膜增生和血管重构，防止受损血管狭窄；该作用可能与其减少和阻止PDGF-BB的产生和活性，以及抑制MMPs的表达和恢复MMPs/TIMPs平衡有关；④通心络能显著抑制球囊损伤后血管内膜增生和血管重构，可能与其保护血管内皮，改善内皮功能，增加血清NO含量有关；⑤通心络抑制内膜增生和血管重构，减轻受损血管狭窄，还可能是通过抑制NF-κB的活化途径而起作用的。

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。

Analysing ustiloxins inhibiting plant cell mitosis The inhibition experiment of growth of garlic radicle showed that there were more cells in the telophase stage in the garlic radicle dealed with culture filtrate of Ustilaginodea virens than those dealed with H2O. The cell volume of the former was bigger than that of the latter. So it seemed that ustiloxins could inhibit the cell mitosis, but not in the cell elongation.

毒素对植物细胞分裂的抑制作用分析：用大蒜根尖做抑制试验，发现用稻曲病菌培养滤液处理过的大蒜根尖呈分裂末期的细胞数目明显多于相同条件浙江大学硕士学位论文下对照的数目，抑制率为69%，且细胞明显比对照的细胞大，说明毒素抑制根尖细胞的有丝分裂，但不能抑制细胞的伸长。

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。

Results The UV-B treatment caused the declines of chlorophyll content, soluble protein content and water content of leaves, besides, dose-effect was existed. The decline of 30 μW/cm^2 treatment was bigger than that of 15 μW/cm^2 treatment. The influences of UV-B radiation on carotenoid content and anthocyanidin content were similar; the change trends were declined firstly then increased. The UV-B treatment with two doses restrained the electron transport of PSⅡ, particularly; the inhibitory effect was biggest after treated 2h, and then this effect was declined in 4, 6 and 8 h, so the dose-effect was existed. The UV-B radiation with two doses restricted photosynthetic rate and the inhibitory effect increased with the increase of treatment time. The high dose treatment caused huge damage to membrane system, while the result of low dose treatment was not obvious.

结果］UV-B处理导致叶绿素、可溶性蛋白含量以及含水量都降低，且存在剂量效应，30μW/平方公分处理的降幅大于15μW/平方公分；UV-B辐射处理对类胡萝卜素含量的影响与花青素相同，均表现为先下降后上升的趋势，2种剂量间差异不大；2种剂量的UV-B处理均抑制了PSⅡ的电子传递，尤其是处理2 h的抑制作用最大，4、6和8 h的抑制作用有所缓解，且存在剂量效应；2种剂量的UV-B辐射均抑制了叶片的光合速率，随着照射时间的延长抑制效应加大；高剂量UV-B处理对膜系统的损伤较大，低剂量UV-B处理结果不明显。

objective effects of plant tannins,chebulinic acid and tellimagrandin i on chemically induced hemoglobin synthesis in k562 cells were investigated.methods the hemoglobin synthesis situation was assayed with benzidine staining.erythroid antigens glycophorin a expression on the surface of k562 cells was labeled by direct immunofluorescence using fluorescein isothiocyanate-conjugated anti-gpa antibodies.then flow cytometric analysis was performed to detect gpa expression levels on surface of the cells.results both chebulinic acid and tellimagrandin i could inhibit the hemoglobin synthesis of butyric acid and hemin-treated k562 cells in a concentration-dependant manner.however,the ba-induced k562 cells were more sensitive to two tannins than heroin-induced cells.conclusion chebulinic acid and tellimagrandin i have inhibitory effect on the erythroid differentiation.

目的 研究可水解单宁诃子酸和特里马素i对氯化高铁血红素和丁酸钠诱导k562细胞红系分化的影响。方法四甲基偶氮噻唑蓝法分析诃子酸和特里马素i对k562细胞生长的影响，联苯胺染色法检测血红蛋白合成情况，应用免疫荧光和流式细胞术检测血型糖蛋白a在细胞表面的表达。结果诃子酸和特里马素i在0.04～0.09？mmol／l浓度下均可显著抑制k562细胞的生长增殖。2种单宁化合物(0.002～0.01？mmol／l)可显著抑制丁酸钠诱导的k562细胞血红蛋白合成，2种单宁化合物(0.01～0.05？mmol／l)还可显著抑制氯化高铁血红素诱导的血红蛋白合成，特里马素i(0.01？mmol／l)还抑制丁酸钠诱导的gpa在细胞表面表达。结论诃子酸和特里马素i对红系分化有抑制作用。

The insulation of apparatus in the power system is often broken by the very fast transient overvoltagewhich is caused by the operation of disconnector in gas insulate substation In this paper, a new idea for the suppressing VFTO by ferrite is put forward, and the characteristic of ferrite is analyzed.

GIS中隔离开关操作时产生的特快速暂态过电压对电力系统及其设备的绝缘具有巨大的破坏力，本文提出了采用铁氧体来抑制GIS中隔离开关操作时产生VFTO的方法，分析铁氧体抑制VFTO的优点，对VFTO的抑制效果进行了实验研究和仿真分析，探讨了具有理想抑制效果的铁氧体参数的具体要求和对理想抑制参数的铁氧体尺寸的估算方法。

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。

What are your goals and strategies for growth?

你的成长目标和策略是什么？

And unto the angel of the church in Sardis write; These things saith he that hath the seven irits of God, and the seven star I know thy works, that thou hast a name that thou livest, and art dead.

3：1 你要写信给撒狄教会的使者，说，那有神的七灵和七星的，说，我知道你的行为，按名你是活的，其实是死的。