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Company main products has: ZYB Multifunction Vacuum Oil Machine, BZJ Oil transformer oil machine (oil temperature automatic control, drop acid, desulfurization, decolorization), QZJ Oil multifunction machine (deacidification, bleaching, automatic control temperature), LPD light oil purification separation device, PWR type Decoloration renewable purification devices, BLY-type plate and frame filter, such as modulartanker.

公司主要产品有:ZYB多功能真空净油机、BZJ变压器油净油机(油温自动控制、降酸、脱硫、脱色)、QZJ多功能净油机(脱酸、脱色、油温自动控制)、LPD轻质油净化分离装置、PWR型脱色再生净化装置、BLY型板框滤芯组合式滤油加油机等。

The aroma components of blood orange fruit were extracted by headspace solid phase microextraction and investigated by gas chromatography-mass spectrometry with two GC columns of different polarity(HP-5 and DB-WAX).

采用顶空固相微萃取对血橙的香气成分进行提取,用两个不同极性的色谱柱(HP-5和DB-WAX)进行分离,利用气相色谱-质谱联用技术对香气成分进行分析。

The main clinical syndrome of kidney deficiency with blood stasis type are easy to wake,forgettery,waist and knee ache,operation wound numbness, suffering upper limb numbness,excessive dream,fatigue,agitated and easy anger,hectic fever,undersexed,dry mouth,insomnia,wine catamenia color, dismal tongue,venation under the tongue is wine,tongue moss are infertile, a thin pulse.

脾肾两虚型主要表现为面色萎黄、腰膝酸痛、潮热、体倦乏力、健忘、自汗、烦躁易怒、患侧上肢麻木、舌质淡、舌苔薄、脉弦、脉细;有病无证型为乳腺癌术后,无明显不适,舌质淡、舌苔薄、脉弦或细;肾虚血瘀型主要主要表现为腰膝酸痛、健忘、易醒、术口麻木、患侧上肢麻木、经色暗红、多梦、体倦乏力、烦躁易怒、潮热、性欲减退、口干、失眠、舌质暗、舌下脉络青紫、舌苔薄、脉细。

The HPLC methods for analysis of N--ribitylxylidine and N-methyl glucamine were established. After optimizing the operation conditions, the principal product and main impurities were well separated. And they were determined by LC-MS. The operation condition of N--ribitylxylidine is, columniation temperature is 30℃, flow rate is 0.7mL/min, UV wave is 244nm, the mobile phase is methanol: water=40: 60 .

首次建立了对葡甲胺和核糖胺的高效液相色谱分析方法,通过对色谱操作条件的优化,成功分离了主产物和杂质,在此条件下,应用液相色谱-质谱联用仪对糖基胺及生成杂质进行了指派定性,并测定了两种糖基胺及其主要杂质的含量,获得了满意的结果。

Methods The cells were divided into 5 treatment groups(10,25,50,75 and 100 μmol·L-1 QUE), blank control and menstruum control group. The rat C6 cells were cultivated to 1×106·mL-1 in the RPMI 1640 medium, then added into 96 holes board with various doses of QUE by 3 holes per group,and MTT assay was used to observe the proliferation of the cells treated for 24,48 and 72 h. The change of cell cycle was also observed by flow cytometry after the cells were treated with 50 and 100 μmol·L-1 QUE for 48 h. The changes of the protein P53 and Bcl-2 of C6 cells treated with 50 μmol·L-1 QUE for 48 h were detected by immunocytochemical methods.

按QUE浓度分成10、25、50、75及100 μmol·L-15个处理组和空白对照组及溶剂对照组,大鼠脑胶质瘤C6细胞在RPMI 1640培养基中生长达1×106·mL-1后,在96孔板中分别加入上述浓度的QUE继续培养,每组设3复孔,作用24、48及72 h,采用MTT比色法检测QUE对大鼠脑胶质瘤C6细胞的增殖抑制情况,流式细胞术对50及100 μmol·L-1的QUE作用48 h的大鼠脑胶质瘤C6细胞进行周期分析,免疫组化法检测50 μmol·L-1的QUE作用48 h 的p53和bcl-2基因产物。

Methods SH-SY5Y cells, a human neuroblastoma cell line, were incubated with different concentrations of fluoride for 48 hr and somle of them were treated with vitamin E precedently. The functional situation of cells was measured by MTT method; lipid peroxidation was detected by High-Performance Liquid Chromatography; phospholipid was separated by a Silica SepPak cartridge and neutral lipids by HPLC.

体外培养SH-SY5Y人脑神经母细胞瘤细胞,在培养液中加入不同浓度的氟化物或加入抗氧化剂,培养48h后用测定细胞MTT的方法来了解细胞的损伤程度,用高效液相色谱法分离和测定培养液中脂质过氧化物水平,用过柱和比色法测定细胞生物膜磷脂含量,用高效液相色谱法测定细胞生物膜辅酶Q和胆固醇含量。

Light microscope and transmission electron microscopy showed that SMMC-7721 cells induced by SAHA had undergone the restorational alteration in morphology and ultrastructure, which were different from those of nontreated cells but were similar to those of normal cells, and the changes were as follows: the cells turned to be flat and spread; the nucleo-cytoplasmic ratio lessened and nuclear shape became rather regular; the number of nucleolus reduced and its volume lessened; euchromatin increased while heterochromatin decreased in nucleus; in the cytoplasm, mitochondria grew in number with relatively consistent structure and well-developed mitochondria cristae; Golgi complex turned to be well-developed and typical; rough endoplasmic reticulum increased. Immunocytochemistry assay showed that the expression of AFP and PCNA were declined significantly. FCM analysis showed SAHA could arrest SMMC-7721 cells in G0/G1 phase, with an accumulation of the cells in G0/G1 phase while a decrease of cells in S phase. Semi-quantitative RT-PCR detection revealed that the expression of p21WAFl mRNA was upregulated remarkably in the cells treated with SAHA.

结果:倒置显微镜和透射电镜观察显示,经SAHA处理的细胞增殖速度显著减慢,细胞体积增大,细胞核较小,形状较为规则,核仁数量减少、体积变小,核内常染色质增多而异染色质减少,核质比例减小,细胞质内线粒体数量增多、线粒体嵴发达,高尔基体较为典型,粗糙型内质网增多,呈现出与正常上皮细胞相似的形态变化;MTT比色法测定结果显示不同浓度(2.5、5.0、7.5、10.0uM)SAHA对SMMC-7721细胞的增殖均有抑制作用,并有明显的剂量依赖和时间依赖关系;免疫细胞化学检测显示SAHA能显著降低PCNA和AFP在SMMC-7721细胞中的表达;流式细胞仪检测结果显示,SMMC-7721细胞经SAHA处理后,G0/G1期细胞明显增加,S期细胞则明显减少,细胞被阻滞于G0/G1期;RT-PCR检测结果表明,SAHA作用12h后SMMC-7721细胞中p21WAF1 mRNA的表达即有增加,24h后更为明显。

The main intermediates were detected during decomposition,such as acetic acid,oxalic acid,malonic acid,phenol,3-hydroxyhypnone,naphthalene,benzene sulfonic acid,phthalic acid,β-naphthalene etc . by ultraviolet-visiblespectroscopy,ion chromatographand gas chromatograph coupled with mass spectrophotometertechniques.The possible degradation pathway of Acid Orange Ⅱ was also speculated,that was,hydroxyl radical reacted with the azo linkage-bearing carbon of naphthol-ring,and the C—N cleaved,the azo-dye decolored and mineralized.

运用紫外光谱、离子色谱、色谱-质谱联用等方法,测定出酸性橙Ⅱ的主要降解产物有乙酸、乙二酸、丙二酸、苯酚、3-羟基苯乙酮、萘、苯磺酸、邻苯二甲酸、β-萘酚等,并依此推测酸性橙Ⅱ的降解机理,即羟基自由基攻击酸性橙Ⅱ分子上与萘环相连的C—N键,导致C—N键的断裂,进而染料脱色矿化。

The water and oil are removed from soybean oil degummed residues, and then separated into two parts by using 95% ethanol extraction.

为促进和拓宽磷脂在医药学领域的应用,进行了锆镁基质脂质体色谱固定相制各及药物与脂质膜相互作用研究。

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。

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