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In this method, we use the pooled correlogram based on human auditory model to extract the pitch of speech. An unsupervised lateral inhibitory network is used to get the peak position, which simulates the lateral inhibitory phenomenon in human auditory system.

采用基于人耳听觉模型的相关图来提取语音信号的基频,运用无监督的侧抑制神经网络来模拟人耳侧抑制属性进行基频检测,为了克服在低信噪比情况下侧抑制神经网络的误判问题,引入了相邻语音帧的语音基频的帧间约束。

Porphyrin nitrogen mustard has distinctive effect on the synthesis of DNA and photodynamic anti-tumor activity.

卟啉氮芥可显著抑制人肝癌细胞SMMC7721DNA的合成;对人肝癌细胞SMMC7721有显著的光动力抑制作用,可破坏肿瘤细胞的细胞膜,抑制肿瘤细胞DNA的合成。

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

DCs acquired by our reformed methods express both CD83 and CD 14 molecules highly, and have a higher density than other domestic reports. The higher TNF in DCs culture medium of HC patient suggests DCs in patient still have antigen presenting ability and by optimization the culture medium would improve its presenting ability and have a potential value in design and application individual vaccine. Although antigens pulsed DCs have a decrescent antigen presenting ability but BCG HSP70 could induce its mature and improve its presenting ability. Suggests BCG HSP70 would be a useful mature inducer. Lymphocytes primed by DCs based HC vaccine have the specific cytotoxicity against HCC lines. The CTL after freezing and anabiotic could prophylaxis and therapy HC xenograft on nude mouse. The results also suggests that CD4〓 lymphocytes play a important role in HC with a good differentiation and would be useful in treatment this kind of HC. After being activated by Peptide LLNQHACAV of hAFP and apoptotic HCCs pulsed DCs respectively, the culture medium of activated lymphocytes both contains a high level Th1 cytokines IL-12 and TNF. Primed lymphocytes appeared a characteristic of NK cells. DCs not only inhibited the growth of human HCC and other cancer cells in vitro but also prevented the growth of HC xenograft on nude mouse in vivo. There are at least three kinds of mechanism playing important role in DC based vaccine ,there are inhibition of DCs, HC specific CTL and cytokines pathway.

诱导出的DC共同表达CD83和CD14分子,CD83分子表达明显高于国内报道;肝癌患者DC培养上清中TNF水平高于健康人,提示肝癌患者DC仍具一定的抗原呈递能力,适当调控可使其行使APC功能,以期在肝癌个体化疫苗中发挥作用;DC负载肝癌可溶性抗原后,抗原呈递能力降低,BCG HSP70可促进DC成熟,增加其抗原呈递能力,预示BCG HSP70有可能成为促进DC活化和成熟的另一重要分子;肝癌DC疫苗在体外诱导肝癌特异性淋巴细胞,活化的淋巴细胞在体外对肝癌细胞的杀伤以特异性CTL为主,同时分泌较高水平Th1型细胞因子IL-12和TNF,并抑制4种肝癌细胞生长;冷冻复苏后的肝癌特异性淋巴细胞可以预防和抑制人肝癌裸鼠皮下移植瘤,提示DC负载肝癌可溶性抗原后诱发的MHC-Ⅱ类限制性CD4〓T细胞有可能在分化程度高的肝癌治疗中发挥作用;用DC和HLA-A2〓DC分别负载凋亡肝癌细胞和hAFP218-226位LLNQHACAV HLA-A2限制性九肽,在体外诱导肝癌特异性淋巴细胞,活化后的CTL细胞分泌较高水平的Th1型细胞因子IL-12和TNF,并具较强杀伤活性,此CTL同时具备NK细胞特征;DC对肿瘤细胞的抑制作用可能是通过吞噬实现的,Fas-L在DC抑制中也起一定作用;DC对人肝癌裸鼠皮下移植瘤的抑制率为97%;在肝癌DC疫苗的作用中,至少联合3种以上机制,即通过DC的直接作用、肝癌特异性CTL和细胞因子途径直接或间接地杀伤和抑制肝癌细胞。

That means Pho85 kinaseand calcineurin were involved in salt tolerance with an identical target protein or in 中科院上海生化与细胞所博士学位论文摘要 the same pathway. Inhibition of calcineurin decrease the YPH499, pho80? mutant,and pap1 (pcl7)? mutant Mn2+ tolerance but not that of pho85? mutant and thepho85? mutant was more sensitive to Mn2+ than YPH499, pho80? mutant, and pap1(pcl7)? mutant even with the addition of cyclosporin A. Therefore, the conclusioncould be drawn that PHO85 gene played a dominant role in Mn2+ homeostasisregulation in compare with calcineurin. As for Ca2+ tolerance, cyclosporin A canincrease the tolerance to Ca2+ of all the mutant mention above, that means Pho85kinase and calcineurin function antagonistically in regulation of Ca2+ homeostasis.In Bioinformatics, BRI3 gene is a novel gene without any function clue but givehigh conservation in mammalian.

我们通过钙调磷酸酶的特异抑制剂环孢菌素A研究了YPH499、+2+pho85缺失株、pho80缺失株、pap1缺失株在钙调磷酸酶失活后对Na、Mn、2+Ca金属离子敏感性的变化,结果显示Pho85蛋白激酶和钙调磷酸酶通过直接+或间接激活同一个靶蛋白或途径来增强细胞对Na的耐受;和钙调磷酸酶相比,2+PHO85的缺失对酵母细胞Mn耐受性的破坏是相对控制性的,钙调磷酸酶的失2+活不能进一步降低pho85缺失株对Mn的耐受能力;Pho85和钙调磷酸酶在对2+Ca的耐受调节中是相互拮抗的,钙调磷酸酶的失活能增加pho85缺失株和2+pho80缺失株的Ca耐受。i中科院上海生化与细胞所博士学位论文摘要对本实验室克隆的人新基因BRI3进行系统的生物信息学分析,发现它是一个在哺乳动物中保守的,但功能未知的基因。

Results: Tyroserleutide can significantly increase the life span of H22 tumor-bearing mice by 50-70% in dosages of 20ug/kg/d-80ug/kg/d,specially the high dosage of 80ug/ml can significantly increase the life span by 69.24%; Tyroserleutide can inhibit the growth of transplanted hepatocellular tumor BEL-7402 in nude mice,the rate of tumor inhibition was25-50% in dosages of 40-320ug/ml ,the inhibition rate of 160ng/ml was 44.03%; Tyroserleutide could inhibit the growth of H22 and BEL-7402 tumor in a dose-dependent manner. Simultaneously, tumoricidal activity of tyroserleutide against BEL-7402 cell line in vitro was observed hinger when compared with the control group(P.05).The inhibition effect of 72hrs was higher than 24hrs,48hrs,96hrs.And specially the high dosage of 160ug/ml can significantly inhibit growth of tumor cell by 19.36%. Tyroserleutide can activated PEM and marked enhance cytotoxicity andphagocytosis functions in vitro and in vivo. The OD values of cytotoxicity were observed hinger when compared with the control group(P.05).The cytotoxicity of macrophages activated by tyroserleutide against BEL-7402 and B16-F10 was 35.58%,61.2% in vitro and21.39%,47.63% in vivo. The cytotoxicity rate of nude mice PEM was 32.86%,73.07% in vivo. Furthermore, tyroserleutide alone could stimulated the production of IL-1B TNF- a and NO by M . Tyroserleutide and LPS could synergistically activated M producing more cytotoxicity effectors. Conclusion: Tyroserleutide had inhibition functions against hepatoma carcinoma .Its possible mechanisms were related to the affect that Tyroserleutide could inhibit tumor cell directively and induce tumor cells apoptosis or death effectively.

结果:酪丝亮肽能显著延长腹水型肝癌H_(22)小鼠的生存时间,给药剂量为80μg/kg/d时疗效最显著,达到69.24%,在20μg/kg/d-80μg/kg/d剂量范围内生命延长率为50-70%,给药剂量与荷瘤鼠生存时间呈现一定量效关系;酪丝亮肽能显著抑制人肝癌BEL-7402移植瘤裸鼠的肿瘤生长,给药剂量为160μg/kg/d时疗效最显著,抑制率为44.03%,并且在40-320μg/kg/d剂量范围内抑制率为25-50%,给药剂量与肿瘤抑制率呈现一定量效关系;酪丝亮肽体外对人肝癌BEL-7402细胞生长有一定的抑制作用,在作用72hrs时各浓度酪丝亮肽对肿瘤细胞的抑制作用较24hrs、48hrs、96hrs明显,其中浓度为100μg/ml时抑制率达19.36%;酪丝亮肽体内外均能增强小鼠腹腔巨噬细胞对肿瘤细胞的杀伤:体外作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强,与效应细胞对照组相比有显著性差异(P<0.05)杀伤率分别达到35.58%、61.2%;体内作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强,与生理盐水对照组相比有显著性差异(P 。05),杀伤率分别达到21.39%、47.63%;裸鼠腹腔巨噬细胞经酪丝亮肤作用后对BEL一7402、B 16一F10杀伤功能明显增强,与生理盐水对照组相比有显著性差异(P.05),最高杀伤率分别达到32.86%、73.07%;酪丝亮肤能增强单核巨噬细胞系统的吞噬功能,吞噬指数与生理盐水组比较有显著性差异(P.05);酪丝亮肤体外作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO,与效应细胞对照组相比有显著性差异(P.05);酪丝亮肤体内作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO,与生理盐水对照组相比有显著性差异(P.05);酪丝亮肤能促进鼠巨噬细胞株R戌W264.7分泌合成IL一1p和NO,IL一1日、NO水平分别在酪丝亮肤作用24hrs、12hrs时达到高峰,酪丝亮肤单独应用能提高巨噬细胞的分泌合成功能,而且酪丝亮肤能与LPS协同作用刺激巨噬细胞的细胞毒效应分子分泌合成。

The experiments of the biological activity for target molecula were accomplished. The experiment results of inhibiting activity against COX-2 indicated that the compound TM-II-5f had the highest inhibition rate, up to 95.59%, and yet the compound TM-II-5g exhibits weakly inhibiting activity.

对目标产物TM-II-5a~5g进行了生物活性研究,人环氧酶-2(COX-2)活性抑制实验结果表明:目标产物TM-II-5f对人环氧酶-2(COX-2)有很强的抑制活性,抑制率高达95.59%,目标产物TM-II-5g具有较弱的抑制率(0.61%)。

MTT assay FAK signaling pathway inhibitor genistein on human corneal epithelial cell cytotoxicity;RT-PCR detection of human corneal epithelial cells adhesion to fungus at different times,extracellular matrix protein including laminin,fibronectin,FN glass,Ⅳcollagen,transmembrane protein integrinαⅤ,integrinβ1(ITGβ1),as well as the FAK signaling pathway FAK1,FAK2 and Paxillin gene expression;Western blot detection of the signal transduction pathway adhesion-associated protein ITGβ1,FAK and PAX expression and the inhibition of genistein. Immunocytochemical method was used to observe the LN,FN and FAK expression in human corneal epithelial cells during interaction with the fungues;Laser scanning confocal microscope had a cell positioning on FN,FAK and PAX,observed the changing of the human corneal epithelial cytoskeleton after stimulated by fungues;Quantitatived by flow cytometry to detect of human corneal epithelial cells with PAX at ITGβ1 fungal expression after adhesion;Optical microscopy quantitied the fungues and human corneal epithelial cell adhesion and recorded to determination the integral optical density afrer adhesion;Scanning and transmitted electron microscope observed the changing of cell ultrastructure after fungues and human corneal epithelial cell adhesion.

第一部分真菌激活人角膜上皮细胞FAK信号转导通路的体外实验研究将三种常见致病真菌(白色念珠菌、烟曲霉菌和茄病镰刀菌)分别与人角膜上皮细胞共孵育,MTT法检测FAK信号通路抑制剂染料木黄酮的对人角膜上皮细胞的细胞毒性作用;RT-PCR检测真菌黏附人角膜上皮细胞后不同时间细胞外基质层连蛋白、纤连蛋白、玻连蛋白、Ⅳ型胶原、跨膜蛋白整合素αV、整合素β1(ITGβ1),以及FAK信号通路中FAK1、FAK2和桩蛋白基因的表达情况;Western blot的方法检测黏附信号转导途径相关蛋白ITGβ1、FAK和PAX的表达,以及染料木黄酮对真菌刺激人角膜上皮细胞FAK信息通路活化的抑制作用;免疫细胞化学方法观察人角膜上皮细胞与真菌相互作用过程中LN、FN和FAK的表达;激光共聚焦显微镜对FN、FAK和PAX进行了细胞定位,并观察真菌刺激后人角膜上皮细胞骨架的变化;流式细胞仪定量检测人角膜上皮细胞ITGβ1与PAX在真菌黏附后表达的改变;光学显微镜观察真菌与人角膜上皮细胞黏附数量,记录并测定了黏附后积分光密度值OD扫描及投射电镜观察了真菌与人角膜上皮细胞黏附后,细胞超微结构的改变。

The effect of AA on BEL-7402 was not significant; However, AA could effectively enhance AT-induced hepatocarcinoma cell apoptosis and lesion severity through activation of caspase-3 but not ERKs-Conclusion; Caspase-3 and ERKs proteins could involve in arsenic-induced hepatocarcinoma cell apoptosis and differentiation respectively as intracellular signaling molecules; The effect between AT and AA on hepatocarcinoma is synergistic, which further inhibits cell growth and induces apoptosis in human hepatocarcinoma cells through activation of caspase-3 but not ERRs.

AA对BEL-7402无明显的作用,但能有效的通过caspase-3而不是ERKs的激活促进AT对肝癌细胞的凋亡效应。结论:ERKs和caspse-3信号蛋白可能分别参与了砷剂诱导的人肝癌细胞促分化和凋亡效应,AT和AA对肝癌细胞的作用有协同性,他们通过caaspase-3而不是ERKs的激活进一步抑制了肝癌的生长,诱导其凋亡。

If you like blue,you are a withdrawn person.You don't like to talk with others and you would rather be along in a lonely place.Your self-repression is very strong.Although you meet exciting things,yu will be calm.you can keep a mediocrity heart.You have a good sense of opinion.You pay attention to details.You don't have very good purpose.It's very good for you to live in a placid life.

如果你喜欢蓝色,你是性格内向的人,你不太喜欢与别人交流,宁可找个僻静的地方独处;你的自我抑制能力很强,即使遇到令人激动的事,你也能不为所动,保持一颗平常心你有较强的判断力,能看到别人不注意的方面;你的目标不算很远大,对你来说,安安稳稳过着平静的生活是最理想不过的了。

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According to the clear water experiment, aeration performance of the new equipment is good with high total oxygen transfer coefficient and oxygen utilization ratio.

曝气设备的动力效率在叶轮转速为120rpm~150rpm时取得最大值,此时氧利用率和充氧能力也具有较高值。

The environmental stability of that world - including its crushing pressures and icy darkness - means that some of its most famous inhabitants have survived for eons as evolutionary throwbacks, their bodies undergoing little change.

稳定的海底环境─包括能把人压扁的压力和冰冷的黑暗─意谓海底某些最知名的栖居生物已以演化返祖的样态活了万世,形体几无变化。

When I was in school, the rabbi explained everythingin the Bible two different ways.

当我上学的时候,老师解释《圣经》用两种不同的方法。