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However, the surplus residual chlorine can affect people's taste and smell, destroy the quality of water. Moreover, in the process of disinfection, chlorine can react with organic matter and produce a series of hydrochloric ether such as chloroform, bromoform, bromodichloromethane, chlorodibromomethane and so on, these matters can cause to some extent cancer to human body.

但是,水中过量的余氯会影响水的口感和气味,破坏水的品质;此外,在消毒过程中,氯与水中残余的有机物产生化学作用,生成一系列氯代烃如三氯甲烷、溴仿、溴二氯甲烷、氯二溴甲烷等,这些物质会对人体产生一定程度的致癌作用;对于以自然水源作为生活用水来源的城市必然要对水加氯消毒后才可使用。

Each starch reagent has its own mode of action on mineral surface, such as primary starch mainly by hydrogen bond, cationic starch by the co-action of hydrogen bond and electrostatic force (for minerals with negative charge on its surface), while carboxymethyl starch, hydroxamic acid starch and dialdehyde starch principally by chemical force accompanied with hydrogen bond and electrostatic force in part. Such chemical forces ensure the close adsorption of reagent on diaspore surface and enforces the hydrophilic of mineral surface. Also the branched chain enable the starch to cover the collector adsorbed on mineral surface, so as to depress diaspore furthermore.

不同淀粉药剂在矿物表面表现不同作用,原淀粉主要是氢键的作用,阳离子淀粉是氢键和静电力的共同作用,羧甲基淀粉、羟肟酸淀粉和双醛淀粉离子性药剂与矿物间的作用除了氢键、静电力外,更重要的是与矿物表面金属离子间产生的化学作用,使药剂能牢固地吸附在一水硬铝石矿物表面,增加矿物表面的亲水性,同时,淀粉支链结构的存在,使它能够掩盖吸附的捕收剂,达到抑制一水硬铝石的目的。

It is included that 4-5 types of active sites exist in the catalytic system and the active site produced polymer with low molecular weight is easy to be activiated while TEA is used as the cocatalyst. While TIBA, the active site produced polymer with high molecular weight and seldom active site produced polymer with low one is prone to be activiated. MAO tends to activiate the active site produced polymer with middle-level molecular weight. In TEA-TIBA catalytic system, TEA and TIBA activiate the corresponding active site and the weight of every active site gradationally varied with the change of the ratio of the two cocatalysts. And the activity of the active site produced polymer with high molecular weight is proportion to the concentration of TIBA.

发现:TEA作为助催化剂时产生低分子量产物的活性中心易于活化,且体系中具有活性的活性中心有4~5种;TIBA易于活化产生高分子量的活性中心,基本上不能活化产生低分子量产物的活性中心;MAO对产生中等分子量产物的活性中心活化能力较强;在TEA-TIBA混合物体系中,TEA和TIBA各自对活性中心的作用表现为明显的互补现象,各活性中心的相对强度随着两种助催化剂之间的比例改变呈现渐次变化,其中产生高分子量产物的活性中心的相对活性(来源:c5AB3fC论文网www.abclunwen.com)与TIBA的浓度有明显的正相关性。

Intravoneous injection of 0.5mg/kgBW jingsongling cause the 60 minutesrelaxation of goat gastric motor.The effects of jingsongling on the gastric motor ofgoat is major of effects of α2 -adrenoceptor agonist,as well as that of α1 -adrenoceptor agonist,the effects of α1 -adrenoceptor agonist concentrate at thecardic and pylorus;the function of α2 -adrenoceptor exit widely at cardic,pylorus,rumen,reticulum,omasum and abomasum,the function at different part is not the same.The lowestdose of jingsonglinginhibiting the amplitude and frequency of the gastricmyoelectric is 0.01mg/kgBW;the influence of jingsonglingto the gastricmotility of goat is dose-dependent,and the amplitude regain after the frequency ofgastric myoelectriv wave.When the goat revived,the gastric motor function is notreach the level of the normal;the major reason ofjingsongling cause the goat gastricrelaxation is the amplitude renew slowly.The intravoneous injection ofjingsonglingfirst,after 5 minutes,intravoneous injection the antagonist,the effect of prazosin and idazoxan mixed is best,which can fast reversal of theinhibition of jingsongling on the gastric motor of goat,the effects of idazoxan isgood,and the prazosin block the effection of jingsongling is better than that ofxylazine,especially at cardia and pylorus.When intravoneous injection of0.5mg/kgBW idazoxan and/or prazosin only,the amplitude of gastric myoelectric ingoat increases at a certain degree,but the frequency is not changed.

静脉注射0.5mk/kgBW的静松灵引起山羊胃蠕动弛缓长达60分钟;静脉注射0.5mg/kgBW的静松灵对山羊胃蠕动机能的影响是以α2肾上腺素受体作用为主的,兼有α1肾上腺素受体的作用,而且静松灵的α1肾上腺素受体的作用主要集中在幽门和贲门;α2肾上腺素受体的作用广泛存在于贲门、瘤胃、网胃、瓣胃、皱胃和幽门中,不同部位间有功能上的差异;静注0.01mg/kgBW的静松灵是对山羊的贲门、瘤胃、网胃、瓣胃、皱胃和幽门的肌电波频率和振幅均产生影响的最低剂量;静注一定剂量的静松灵对山羊胃蠕动的抑制作用与剂量呈相关性;而且山羊胃肌电波振幅的恢复比肌电波频率的恢复慢;苏醒时山羊的胃蠕动机能尚未恢复到正常状态;静松灵引起山羊胃弛缓的主要原因是由于胃肌电波的振幅恢复慢;静注0.5mg/kgBW的静松灵,5分钟后静注0.5mg/kgBW的拮抗剂时,咪唑克生+哌唑嗪的作用最好,能迅速地逆转静松灵对山羊胃蠕动的抑制作用,咪唑克生也有很强的拮抗作用,而哌唑嗪对静松灵的拮抗效果好于对隆朋的拮抗;单独静注0.5mg/kgBW的咪唑克生和/或哌唑嗪时,山羊的瘤胃、网胃、瓣胃、皱胃、贲门和幽门的肌电波振幅有一定程度的增强,而肌电波频率未见变化。

From the perfusion experiments with isolated rabbit heart and vessels were obtained the follow- ing results:(1)Potassium antimony tartrate produced depression of the isolated rabbit heart,and this depressant action became more marked when the pH of the solution was raised from the original value of 5.4 to that of 7.2;(2)At the same pH levels,the cardiac action of the potassium salt was slightly stronger than that of the corresponding sodium salt;(3)The slight vase-dilator effect of potass- ium anti...

从离体器官的灌注实验得到下列结果:(1)酒石酸锑钾对离体兎心有抑制作用,将其pH 从5.4调整到7.2时,作用亦随以增加。(2)在相同 pH 时,酒石酸锑钾的心臓抑制作用较酒石酸锑钠略强。(3)酒石酸锑钾对离体兎耳血管的轻微扩张作用,系由于该药溶液的微酸性反应,当将药液 pH 调整至7后即无作用。(4)对于离体兎肺血管则不问 pH 为4.8或7,均产生轻微的血管收缩作用。

The thesis also discussed the synthetic influence of above factors on dynamic diagenesis in detail and graded dynamic diagenesis into three types, which were respectively thermally dynamic diagenesis, tectonically dynamic diagenesis and hydrokinetic diagenesis, and then the types of diagenesis controlled by dynamic factors had been studied: 1 thermally dynamic diagenesis, clarified the ration relationship by the conception of the thermally evolving track and the thermally maturity, 2 tectonically dynamic diagenesis, changed the porosity of reservoir mainly by tectonically movement;3 . hydrokinetic diagenesis, changed the physical and chemical properties resist-press intensity of the rock by the participating of liquid.

在研究以上控制因素的基础上,将成岩动力作用分为热动力、构造动力、流体动力成岩作用三种类型:1、热动力成岩作用,运用热演化轨迹和热成熟度的概念研究与成岩作用之间的定量关系,砂岩孔隙度随热成熟度增加而呈指数减小;2、构造动力成岩作用,盆地构造变形可以使砂岩的孔隙体积在相对短的时间内产生明显的变化,构造滑脱推覆作用比水平侧向挤压作用压实减孔量小,可保留更多的孔隙度;3、流体动力成岩作用,化学成岩反应是在流体参与下完成的,它改变了岩石的物理化学性质,改变了岩石的抗压强度。

The paper studied the scavenging active oxygen radicals of brown pigment from chestnut shell. The results showed that the brown pigment had scavenging effects on hydroxyl radical, superoxide anion radical and aliphatic radicals on lipid-peroxidation. In the range of test concentration, the maximum scavenging or inhibition rate of the brown pigment to hydroxyl radical generated by Fenton reaction, superoxide anion radical generated by illuminating riboflavin system and linoleic acid auto-oxidation was 83.0%, 82.1% and 88.5% respectively.

从清除羟基自由基和超氧阴离子自由基、抗脂质过氧化以及还原能力等方面对板栗壳棕色素的抗活性氧自由基进行了试验研究和评价,结果表明:板栗壳棕色素对Fenton反应产生的羟基自由基和光照核黄素产生的超氧阴离子自由基均具有较强清除作用,对脂质过氧化过程中产生的脂自由基和脂过氧化自由基有明显的抑制作用,且在试验浓度范围内,其最大清除率或抑制率分别可达到83.0%、82.1%和88.5%。

The shear layer vortices dominate in the initial portion of the jet, which are a result of the K-H instability. The crossflow encounters an adverse pressure gradient ahead of the jet and separates to form horseshoe vortices under the pressure downstream, and they develop into the wake. The wake vorticity comes into being in the actions of an adverse pressure gradient and a wall-normal component of vorticity, which originates from the wall boundary and is entrained into the jet. The shear layer vortices encounter adverse pressure gradients in the lee of the jet and break down, leading to the formation of the CVP and the CVP is the most important characteristic of the jet in crossflow.

文中指出:剪切层涡源于射流与横流之间的K-H不稳定性;马蹄形涡的产生是由于射流喷口上游迎风侧的壁面边界层内存在逆压梯度,使流动发生了分离,在下游逆压梯度的挤压作用下,形成了马蹄形涡,马蹄形涡向下游发展,进入尾迹区;在逆压梯度和法向涡生成项的共同作用下产生了尾迹涡,尾迹涡源于壁面边界层,止于射流,并将部分涡量向上输运至射流内部的CVP;CVP是横向紊动射流的重要特征,剪切层涡破裂后,在逆压梯度的作用下CVP形成。

The effects and mechanism of GABAergic neurons, NOergic neurons, opioid peptide and cyclic adenosine monophosphate in the nucleus reticularis thalami on sleep-wakefulness cycle of rats and the effects and mechanism of the 5-HTergic nerve fibers project from the nucleus raphes dorsalis to RT on sleep-wakefulness cycle of rats were investigated with the methods of brain stereotaxic, nucleus spile, microinjection and polysomngraphy.1. The effects of GABAergic neurons in RT on sleep-wakefulness cycle of rats1.1 Microinjection of 3-mercaptopropionic acid (3-MP, a kind of glutamate decarboxylase inhibitor) into RT. On the day of microinjection, sleep only decreased a litter. On the second day, sleep marked decreased and wakefulness marked increased. On the third and fourth day, sleep and wakefulness stages resumed to normal.1.2 Microinjection of gamma-amino butyric acid (GABA 1.0μg) into RT enhanced sleep and reduced wakefulness compared with control; while microinjection of L-glutamate (L-Glu, 0.2μg) decreased sleep and increased wakefulness; microinjection of bicuculline (BIC, 1.0μg), a GABAA receptor antagonist, enhanced wakefulness and reduced sleep; microinjection of baclofen (BAC, 1.0μg), GABAB receptor agonist, had the same effects as GABA.2. The effects of NOergic neurons in RT on sleep-wakefulness cycle of rats2.1 Microinjection of L-arginine (L-Arg, 0.5μg) into RT decreased sleep compared with control, but there were on statistaical difference between L-Arg group and control; while microinjection of sodium nitroprusside (SNP, 0.2μg), a NO donor into RT, sleep marked decreased and wakefulness marked increased. Microinjection of nitric oxide synthase inhibitor, N-nitro-L-arginine (L-NNA, 2.0μg) into RT enhanced sleep and reduced wakefulness.2.2 After simultaneous microinjection of L-NNA (2.0μg) and SNP (0.2μg) into RT, SNP abolished the sleep-promoting effect of L-NNA compared with L-NNA group; after simultaneous microinjection of L-NNA (2.0μg) and L-Arg(0.5μg) into RT, we found that L-NNA could not blocked the wakefulness-promoting effect of L-Arg.3. The effects of opioid peptide in RT on sleep-wakefulness cycle of rats3.1 Microinjection of morphine sulfate (MOR, 1.0μg) into RT increased wakefulness and decreased sleep compared with control; while microinjection of naloxone hydrochloride (NAL, 1.0μg), the antagonist of opiate receptors, into RT, enhanced sleep and reduced wakefulness.3.2 After simultaneous microinjection of MOR (1.0μg) and NAL (1.0μg) into RT, the wakefulness-promoting effect of MOR and the sleep-promoting effect of NAL were not observed compared with control.4. The effects of cAMP in RT on sleep-wakefulness cycle of rats Microinjection of cAMP (1.0μg) into RT increased sleep and decreased wakefulness compared with control; microinjection of methylene blue (MB,1.0μg) into RT enhanced sleep and reduced wakefulness compared with control.5. The effects of the 5-HTergic nerve fibers project from DRN to RT on sleep-wakefulness cycle of rats5.1 When L-Glu (0.2μg) was microinjected into DRN and normal sodium (NS,1.0μg) was microinjected into bilateral RT. We found that sleep was decreased and wakefulness was increased compared with control; when L-Glu (0.2μg) was microinjected into DRN and methysergide (MS,1.0μg), a non-selective 5-HT antagonist, was microinjected into bilateral RT, We found that sleep was enhanced and wakefulness was reduced compared with L-Glu group.5.2 When p-chlorophenylalanine (PCPA, 10μg) was microinjected into DRN and NS (1.0μg) was microinjected into bilateral RT, We found that sleep was increased and wakefulness was decreased compared with control; microinjection of 5-hydroxytryptaphan (5-HTP, 1.0μg), which can convert to 5-HT by the enzyme tryptophane hydroxylase and enhance 5-HT into bilateral RT, could block the effect of microinjection of PCPA into DRN on sleep-wakefulness cycle.

本研究采用脑立体定位、核团插管、微量注射、多导睡眠描记等方法,研究丘脑网状核(nucleus reticularis thalami,RT)中γ-氨基丁酸(gamma-amino butyric acid ,GABA)能神经元、一氧化氮(nitrogen monoxidum,NO)能神经元、阿片肽类神经递质、环一磷酸腺苷(cyclic adenosine monophosphate,cAMP)及中缝背核(nucleus raphes dorsalis,DRN)至RT的5-羟色胺(5-hydroxytryptamine,5-HT)能神经纤维投射对大鼠睡眠-觉醒周期的影响及其作用机制。1 RT内GABA能神经元对大鼠睡眠-觉醒周期的影响1.1大鼠RT内微量注射GABA合成关键酶抑制剂3-巯基丙酸(3-MP,5μg),注射当天睡眠时间略有减少,第二日睡眠时间显著减少,觉醒时间明显增多,第三、四日睡眠和觉醒时间逐渐恢复至正常。1.2大鼠RT内微量注射GABA受体激动剂GABA( 1.0μg)后,与生理盐水组比较,睡眠时间增加,觉醒时间减少;而RT内微量注射L-谷氨酸(glutamic acid, L-Glu, 0.2μg)后,睡眠时间减少,觉醒时间增加;RT内微量注射GABAA受体阻断剂荷包牡丹碱(bicuculline,BIC,1.0μg)后,睡眠时间减少,觉醒时间增加;RT内微量注射GABAB受体激动剂氯苯氨丁酸(baclofen,BAC,1.0μg)后,产生了与GABA相似的促睡眠效果。2 RT内NO能神经元对大鼠睡眠-觉醒周期的影响2.1大鼠RT内微量注射NO的前体L-精氨酸(L-Arg,0.5μg)后,与生理盐水组对比,睡眠时间略有减少,但无显著性意义;而RT内微量注射NO的供体硝普钠(Sodium Nitroprusside,SNP,0.2μg)后可明显增加觉醒时间,缩短睡眠时间;微量注射一氧化氮合酶抑制剂L-硝基精氨酸(L-arginine,L-NNA,2.0μg)后,引起睡眠时间增多,觉醒时间减少。2.2大鼠RT内同时微量注射L-NNA(2.0μg)和SNP(0.2μg)后与L-NNA组比较发现SNP逆转了L-NNA的促睡眠作用;RT内同时微量注射L-NNA(2.0μg)和L-Arg(0.5μg)后,与L-NNA(2.0μg)组比较发现L-Arg可以增加觉醒而缩短睡眠,其促觉醒作用未能被NOS的抑制剂L-NNA所逆转。3 RT内阿片肽对大鼠睡眠-觉醒周期的影响3.1大鼠RT内微量注射硫酸吗啡(morphine sulfate,MOR,1.0μg)后与生理盐水组对比,睡眠时间减少而觉醒时间增加; RT内微量注射阿片肽受体拮抗剂盐酸纳洛酮(naloxone hydrochloride,NAL,1.0μg)后与生理盐水组比较,睡眠时间增加而觉醒时间减少。3.2大鼠RT内同时微量注射MOR(1.0μg)和NAL(1.0μg)后,与生理盐水组对比,原有的MOR促觉醒效果和NAL的促睡眠效果都没有表现。4 RT内环一磷酸腺苷信使对大鼠睡眠-觉醒周期的影响大鼠RT内微量注射cAMP(1.0μg)后与NS(1.0μg)组比较,睡眠时间增多而觉醒时间减少;RT内微量注射亚甲蓝(methylene blue,MB,1.0μg)后,与NS组比较,睡眠时间增多而觉醒时间减少。5中缝背核投射到丘脑网状核的5-羟色胺能神经纤维对大鼠睡眠-觉醒周期的影响5.1大鼠DRN内微量注射L-Glu(0.2μg),同时在双侧RT内微量注射NS (1.0μg)后,与对照组(DRN和双侧RT注射NS, 0.2μg)比较,睡眠时间减少,觉醒时间增多;大鼠DRN内微量注射L-Glu(0.2μg),同时在双侧RT内微量注射二甲基麦角新碱(methysergide, MS, 1.0μg )后,与对照组(DRN注射L-Glu 0.2μg,双侧RT注射NS 1.0μg)比较,睡眠时间增多,觉醒时间减少。5.2大鼠DRN内微量注射对氯苯丙氨酸(p-chlorophenylalanine,PCPA,10μg),同时在双侧RT内微量注射NS (1.0μg)后,与对照组(DRN和双侧RT注射NS, 1.0μg)比较,睡眠时间增多,觉醒时间减少;大鼠DRN内微量注射PCPA(10μg),产生睡眠增多效应后,在双侧RT内微量注射5-羟色胺酸(5-hydroxytryptaphan , 5-HTP, 1.0μg )后,与对照组(DRN注射PCPA 10μg,双侧RT注射NS 1.0μg)比较,睡眠时间减少,觉醒时间增多。

Results As shown in Western blot analysis, the presence of microsomes did not alter the molecular weight of TM-TNF , but it did result in the cleavage of the IL-2 signal peptide from S-TNFm,suggesting that the leader sequence of TNF might differ from the signal peptide of typical secretory protein in that it seemed not to have undergone cleavage during translation in the rough-faced endoplasmic reticulum. Further enzymatic analysis revealed that TM-TNF was converted into S-TNF through the effect of certain metalloproteinase. Conclusions These results suggest that the mechanisms of TNF-α production may be as follows: Activation of TNF-α producing cells by LPS leads to augmented transcription/translation of TNF-α gene, resulting firstly

实验结果提示17×103 S-TNF产生机制可能是:TNF产生细胞经LPS等激活后,导致TNF基因转录翻译增加,首先形成26×103 TNF,并借助其信号肽疏水氨基酸部分将之&锚定&在细胞膜,成为跨膜型TNF,介导细胞与细胞之间的生物学效应;在某些蛋白酶作用下,可将mTNF的&信号肽&切除,产生17×103分泌型TNF,释放至体液中,在局部或全身发挥作用。

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