查询词典 adenosine

Objective: Our purpose was to study whether exogenous adenosine triphosphate could enter liver cell or not.

目的：研究外源性三磷酸腺苷(adenosine triphosphate，ATP)是否能够进入低温保存大鼠肝脏细胞内。

Objective To study the diagnostic value of adenosine deaminasein all kinds of the pa-tients with liver disease.Methods 212patients of hepatitis in our hospital were selected,135cases were male,and75were female,the average age was（39.6±5.2）years old,in other hand,100blood donors were selected as con-trol group,the value of ADA and the conventional item such as GGT,ALT were determining and a contradistinctive analysis were conducted.Results The item of ADA and the conventional item such as GGT,ALTwere not different in the patients of different kind of liver disease,especially in the patients of chronic persistent hepatitis and chronic active hepatitis,the value of positive rate were92.0%and28.9%,respectively.

目的 测定各类型肝脏疾病病人血清腺苷脱氨酶（adenosine deaminase，ADA）活性值，分析ADA测定结果在各种肝脏疾病中的不同变化，评价ADA测定在肝脏疾病诊断中的应用价值；方法以在我院感染科住院肝炎病人共212例为检测对象，其中男性135例，女性75例，平均年龄（39.6±5.2）岁，以献血员100例为正常对照，对其ADA测定结果进行统计分析，并与传统肝功能检测项目做对比研究；结果 ADA和传统肝功能检测指标在不同类型肝脏疾病中测定值和阳性率各有所不同，特别在慢性活动性肝炎、慢性迁延性肝炎中的阳性检出率有显著不同，分别为92.0%和28.9%，有显著差异（P.01）。

Here we show that phenylarsine oxide and diamide (both were inhibitors for protein tyrosine phosphatases), but not genistein (an inhibitor for protein tyrosine kinases), adenosine, wortmannin and LY294002 (all were inhibitors for phosphatidylinositol 3- and 4-kinases), could inhibit P-selectin exocytosis on activated platelets and could abolish the P-selectin mediated aggregation of activated platelets to neutrophils.

我们发现蛋白酪氨酸磷酸酶的抑制剂phenylarsine oxide和diamide能够抑制P-选凝素从活化的血小板中外排出来，并能够抑制P-选凝素介导的活化的血小板在白细胞表面的粘附，而蛋白酪氨酸激酶的抑制剂genistein，磷脂酰肌醇3-或4-激酶的抑制剂adenosine、wortmannin和LY294002在这些实验中没有作用。

Here we show that phenylarsine oxide and diamide (both were inhibitors for protein tyrosine phosphatases), but not genistein (an inhibitor for protein tyrosine kinases), adenosine, wortmannin and LY294002 (all were inhibitors for phosphatidylinositol 3-and 4-kinases), could inhibit P-selectin exocytosis on activated platelets and could abolish the Pselectin mediated aggregation of activated platelets to neutrophils.

我们发现蛋白酪氨酸磷酸酶的抑制剂phenylarsine oxide和diamide能够抑制P-选凝素从活化的血小板中外排出来，并能够抑制P-选凝素介导的活化的血小板在白细胞表面的粘附，而蛋白酪氨酸激酶的抑制剂genistein，磷脂酰肌醇3-或4-激酶的抑制剂adenosine、wortmannin和LY294002在这些实验中没有作用。

The results obtained are as follows:(1) injection of 50, 100, and 200 nmol/kg adenosine into the renal artery increased the renal afferent nerve activity in a dose-dependent manner with unchanged arterial pressure;(2) pretreatment with 8-cyclopenthl -1,3-dipropylxanthine (DPCPX, 160 nmol/kg), an adenosine A1 receptor antagonist, partly abolished the effect of adenosine; and (3) pretreatment with a nitric oxide synthase inhibitor N w-nitro- L -arginine methylester (L -NAME, 0.1 mmol/kg) significantly enhanced the ARNA response to adenosine.

结果表明：(1)肾动脉内注射50， 100和200 nmol/kg腺苷可呈剂量依赖性地兴奋肾神经传入纤维的活动，而动脉血压不变。(2)肾动脉内预先应用选择性腺苷A1受体阻断剂DPCPX (160 nmol/kg)，可部分阻断腺苷对肾神经传入纤维的兴奋作用。(3)静脉应用一氧化氮合酶抑制剂 L -NAME(0.1 mmol/kg)预处理，延长并增强了肾神经传入纤维对腺苷的反应。

The results obtained are as follows:(1) injection of 50, 100, and 200 nmol/kg adenosine into the renal artery increased the renal afferent nerve activity in a dose-dependent manner with unchanged arterial pressure;(2)pretreatment with 8-cyclopenthl-1,3-dipropylxanthine (DPCPX, 160 nmo//kg), an adenosine A1 receptor antagonist, partly abolished the effect of adenosine; and (3) pretreatment with a nitric oxide synthase inhibitor Nω-nitro-L-arginine methylester (L-NAME, 0.1 mmol/kg)significantly enhanced the ARNA response to adenosine.

结果表明：(1)肾动脉内注射50，100和200nmol/kg腺苷可呈剂量依赖性地兴奋肾神经传入纤维的活动，而动脉血压不变。(2)肾动脉内预先应用选择性腺苷A1受体阻断剂DPCPX(160nmol/kg)，可部分阻断腺苷对肾神经传入纤维的兴奋作用。(3)静脉应用一氧化氮合酶抑制剂L-NAME(0.1mmol/kg)预处理，延长并增强了肾神经传入纤维对腺苷的反应。

The pressor effect of adenosine was due to carotid body cheoreceptor activation. However, a slight increase of ABP induced by intracarotid bolus injection of adenosine following the section of carotid sinus nerves was observed in a few rats, which implied that the central effect might be involved in the pressor effect of adenosine. The delayed effect of adenosine may be attributed to the direct actions (including the negative chronotropic action, thenegative dromotropic action, the negative inotropic action and the vasodilator effect) of adenosine on the heart and blood vessels.

前一效应主要与颈动脉体化学感受器的激活有关，但在少数动物，颈动脉内注射腺苷的升压效应在切除窦神经后并未完全消除，表明腺苷有可能进入神经中枢而发挥作用；后一效应可能由腺苷直接作用于心脏和血管，通过其负性变力、变时、变传导和血管扩张等作用，导致心脏自律性降低，输出量减少和外周阻力下降。

They were two new compounds, [cyclo(Pro-Val-Phe-Phe-Pro-Val-Phe-Ser-Leu),7],[2-N-(1-methoxycarbonylethyl)guanosine, 10], and eight known compounds,(p-hydroxybenzoic acid, 1),(methyl succinate, 2),(russulaceramide, 3),(phenylalanine, 4),(guanine, 5),(β-carboline, 6),(uridine, 8), and (adenosine, 9). All the compounds were isolated from Amanita exitialis for the first time.

分别为：对羟基苯甲酸(p-hydroxybenzoic acid，1)、丁二酸二甲酯(methyl succinate，2)、神经酰胺(russulaceramide，3)、苯丙氨酸（phenylalanine，4）、鸟嘌呤核苷(guanine，5)、β-咔啉(β-carboline，6)、环（脯氨酸-缬氨酸-苯丙氨酸-苯丙氨酸-脯氨酸-缬氨酸-苯丙氨酸-丝氨酸-亮氨酸） [cyclo(Pro-Val-Phe-Phe-Pro-Val-Phe-Ser-Leu)，7]、尿嘧啶核苷(uridine，8)、腺嘌呤核苷(adenosine，9)、2-N-(1-甲氧羰基乙基)鸟苷[2-N-(1-Methoxycarbonylethyl)guanosine， 10]。10个化合物均为首次从致命鹅膏中分离得到，其中化合物7和10为新化合物。

Detail Contents: Genetic disorders -- Immune deficiencies -- Breast cancer -- Colon cancer -- Melanoma -- Cystic fibrosis -- Hemophilia -- Liver disease -- Cardiovascular disease -- Muscular dystrophy -- Alzheimer's disease -- Parkinson's disease -- Huntington's disease -- Viruses: the cornerstone of gene therapy -- Viruses are living crystals -- Viral genomes may be RNA or DNA -- Viruses evolved from plasmids -- Viruses know how to infect cells -- The virus as a gene vehicle -- Viruses used in gene therapy -- Ashi DeSilva: a promising start -- Clinical trials defined -- Cells of the immune system -- Adenosine deaminase -- Preliminary research -- Clinical procedure for ADA gene therapy -- The DeSilva clinical trial -- Jesse Gelsinger: down to earth -- Ornithine transcarbamylase -- Preliminary research -- Clinical procedure for OTC gene therapy -- The Gelsinger clinical trial -- The investigation -- Concluding remarks -- Future prospects -- Safer vehicles -- Reducing immune rejection of the vector -- Improved risk assessment -- Redesigning human anatomy and physiology -- Ethics of gene therapy -- The Belmont report -- Clinical trials -- Physiological enhancement -- Cosmetic applications -- Legal issues -- Regulatory agencies -- The Gelsinger legal trial -- International regulation -- Resource center -- Eucaryote cell primer -- Recombinant DNA primer -- The human genome project -- X-linked severe combined immunodeficiency (SCID-X1)-- Alzheimer's disease -- Huntington's disease.

细节内容︰遗传疾病-免疫的缺乏-乳腺癌-结肠癌-黑瘤-囊性纤维变性-血友症-肝疾病-心血管疾病-肌营养不良-早老性痴呆病-帕金森疾病-亨廷顿疾病-病毒︰基础的基因治疗-病毒在活著水晶--病毒的基因可能是RNA或者DNA --病毒从plasmids被逐步形成--病毒知道怎样感染细胞--作为一辆基因车辆的病毒--基因治疗使用的病毒-Ashi DeSilva︰有希望开始-临床试验确定--细胞的这免疫系统-Adenosine deaminase-初步研究-临床程式给埃达基因治疗--这DeSilva临床试验-婕西Gelsinger︰到地球-Ornithine transcarbamylase-初步研究-临床程式给OTC基因治疗-- Gelsinger临床试验-调查-达成评论-前景-更安全的车辆--矢量的降低免疫的拒绝-改进风险估计-重新设计人解剖学和生理学--伦理学的基因治疗-那些贝拉蒙特报告-临床试验-生理提升-美容应用-法律问题-协调机构-- Gelsinger 合法审讯-国际管理-资源中心人物-Eucaryote信元第一-Recombinant DNA 入门--人类基因工程-- X 连结的严重的结合的免疫缺陷(SCID-X1)-早老性痴呆病--亨廷顿的疾病。

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。

I didn't watch TV last night, because it .

昨晚我没有看电视，因为电视机坏了。

Since this year, in a lot of villages of Beijing, TV of elevator liquid crystal was removed.

今年以来，在北京的很多小区里，电梯液晶电视被撤了下来。