腺苷

Caffeine - A derivative of coffee, is an efficient arouser of central nervous system capable to drive away fatigue, and improve renal circulation. Its stimulation on the cerebral cortex activates Neurotransmitter receptors in the cell membrane; the adenylyl cyclaseactivated on the other surface of the cell catalyzes Adenosine Triphosphate, forming Cyclic adenosine monophosphate, and thus set off series of bio-chemical reactions, like increase of passionate feel, prompt recovery from fatigue after working etc..

咖啡因—由于咖啡本身具有兴奋神经中枢，消除疲劳，增加肾脏血流量的作用，通过对大脑皮层的刺激，使神经递质作用于细胞膜受体，激活了膜另一侧的腺苷酸环化酶，被激活的腺苷酸环化酶催化三磷酸腺苷环化酶，被激活的腺苷酸环化酶催化三磷酸腺苷形成环磷酸腺苷，从而引起一系列生化反应，如增加愉快感和消除事后疲劳等。

Methods Using HIRI model in tabbits,animals were randomly divided into four groups (n=10 in each),HIR group,HIR+ LGT group,HIR+ Pro group and HIR+ LGT+ Pro group,the contents of adenosine triphosphate,adenosine diphosphate,adenosine monophosphate,total adenylic acid numberand energy charge in the liver tissue were measured at 45 minutes after reperfusion, respectively.

复制肝缺血-再灌注损伤模型，随机将40只实验兔分为肝缺血-再灌注组、肝缺血-再灌注＋LGT治疗组、肝缺血-再灌注＋PRO治疗组和肝缺血-再灌注＋LGT＋PRO治疗组。在再灌注45 min时，分别观察肝组织内三磷酸腺苷、二磷酸腺苷、一磷酸腺苷含量、总腺苷酸量、能荷及肝细胞形态学的变化。

METHODS: Based on the antitumor activity and structural feature of 8-chloroadenosine and retinoic acid, modifications were made at positions 5′ and 8,substituted cinnamoyl and benzoyl groups were bound at 8 position through amido and ester bonds, sulfonation and nitrosation at 5′-OH and its direct chlorination were conducted.

对腺苷的8位和8-Cl-腺苷的糖环羟基进行了结构改造，以酰胺键和酯键在腺苷的8位连接了具共轭基团的肉桂酰基和苯甲酰基，得到腺苷的维甲类似物；对8-Cl-腺苷的5′-羟基进行了甲磺酰化，硝基化以及氯代反应，得到了它的衍生物。

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 construction of recombinant UNPase provided a basis for the research on biocatalysed synthesis of adenosine. In comparison with uridine, inosine was the better donar of pentose-1-phosphorate. In the reaction mixture composed of 30 mmolL^(-1)inosine, 10 mmolL^(-1) adenine, and 30 mmolL^(-1) pH 7.5 phosphate buffer and 0.5% wet cells gave a high yield of 85.57% at 60℃ in 3h.

在此基础上研究了不同诱导条件对蛋白表达量的影响分别以肌苷和尿苷为核糖供体研究重组菌转化腺苷的条件，发现肌苷最适合作为核糖供体，在30mmolL^(-1)pH7.5的Na2HPO4-KH2PO4缓冲液中，以30mmolL肌苷和10mmolL^(-1)腺漂呤作底物，加入0.5%基因工程湿菌体60℃反应3h，腺苷的转化率为85.57%。

METHODS: 24 rabbits were divided into four groups: control group; rapid pacing group; adenosine perfusing group; selective adenosine receptor antagonist perfusing group. The index of observed: time of repolarization in monophase action potential (APD90); the active level of A1 adenosine receptor; the level of free calcium in the atrium cells and the ability of atrium cell to release calcium.

新西兰白兔24只，随机分为4组：①对照组：常规克氏液灌流，②腺苷灌流组：灌流液中加入2umol/L的腺苷，③心房快速起搏组：常规克氏液灌流+心房快速起搏，④腺苷受体拮抗剂干预组：克氏液+DPCPX（100nmol/L）灌流+心房快速起搏；观察指标：①起搏前后心房肌单相动作电位复极时间的变化；②起搏组和对照组的心房肌腺苷A〓受体活性对比；③心房肌细胞内游离钙含量以及氯化钾激动后钙释放能力对比。

A mononucleotide,C10H14N5O7P,found in animal cells and reversibly convertible to ADP and ATP;adenosine monophosphate.

一磷酸腺苷单核苷酸，C10H14N5O7P，发现于动物细胞中并能可逆地转化为二磷酸腺苷和三磷酸腺苷；一磷酸腺苷

In pacemaker cells of SA node superfused with the oxygenated K—H solution, MDP, APA, V〓, VDD, RPF and APD〓 were—45±5mv, 48±4mv, 2. 4±0.9v/s, 89±8 mv/s, 200±11bpm and 206±15ms, respectively. Anoxia (perfused for 20min with a modified K—H solution gassed with 100% N〓 and deprived of glucose) increased MDP, APA and V〓, and decreased VDD and RPF in a timedependent manner. At anoxia for 20min, the above parameters were—58±5mv, 64±5mv, 11. 7±2. 7v/s, 24±7mv/s, 92±11bpm and 179± 14ms, respectively. ADase (10U/L).

环戊腺苷和苯基异丙基腺苷不仅能增加豚鼠窦房结起搏细胞APA、MDP和〓，且能减小VDD、RPF和〓在环戊腺苷20nmol／L浓度时，MDA、APA和〓分别增值5.4±0.7mv、7.6±0.9mv和2.4±0.5v／s，VDD、RPF和〓分别降低32±4mv／s、68±9bpm和31±12ms（p.05或0.01）。0.1μmol／L 8—苯茶碱和10μmol／L格列苯脲能明显地抑制环戊腺苷的电生理效应。

Results: 1 Tritiated thymidine incorporation assay showed that 1μM adenosine plus coformycin slightly inhibited CTLL-2 proliferation, while 5-20μM adenosine elicited marked inhibition on CTLL-2 proliferation responded to IL-2 a dose-dependent fashion. 2 Coformycin alone could also inhibit CTLL-2 proliferation at the concentration of 2.5μM. The underlying reason maybe due to the endogenous adenosine produced by CTLL-2 cells.

结果：11μM腺苷对CTLL-2增殖仅有轻微的抑制作用，而5、10、20μM腺苷的存在可显著抑制CTLL-2的增殖，并且呈剂量相关，P值均小于0.05.2CTLL-2经过2.5μM助间型霉素的单独处理也可引起轻度的增殖受抑现象，分析其可能原因是T细胞自身可以分泌腺苷，所以该抑制现象的出现与内源性腺苷有关。3本实验所用腺苷浓度对CTLL-2的活细胞百分率影响轻微。

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。