阿片的

基本解释 (translations)

thebaic

与阿片的相关的网络例句 [注：此内容来源于网络，仅供参考]

Desensitization has been implicated as one of the possible molecular mechanism underlying opioid tolerance and dependence.

阿片受体的脱敏被认为是机体对阿片类药物产生耐受性和成瘾性的分子机制之一。

E. , ACTH antagonizes the analgesia mediated byμand δ opioid receptors, but notκreceptor;(2) The antagonizing effect of ACTH on opioid analgesia is proposed to be mediated by ACTH receptors, although the latter has not been characterized;(3) A contradictory interaction on intracellular cAMP content may constitute one of the postreceptor mechanisms underlying ACTH antagonism of opioid analgesia;(4) Another proposed mechanism of the anti-opioid effect of ACTH is that ACTH can modulate opioid-induced suppression of calcium influx;(5) ACTH has been shown to induce Fos protein expression in selected areas of the rat brain including the nuclei involved in pain regulation as well as the ependyma of the third ventricle and the aqueduct.

根据以上实验结果，本论文首次提出以下论点：（1）ACTH在脊髓水平对抗阿片镇痛具有受体选择性，即ACTH可对抗μ受体和δ受体介导的镇痛，不对抗κ受体所介导的镇痛；（2）由于ACTH与阿片μ受体的肽类配体的结合位点仅有很低的亲和力，与μ受体的非肽类配体的结合位点以及δ受体无亲和力，推测ACTH是通过中枢内的ACTH受体介导发挥抗阿片效应的；（3）ACTH抗阿片作用的受体后作用机制之一是在cAMP信使通路水平与阿片发生相互作用；（4）ACTH抗阿片作用的另一受体后机制是在〓水平影响阿片的效应；（5）通过Fos蛋白的诱导揭示：ACTH可以作用于脑内多个核团，其中包括许多与痛觉调制有关的核团，推测ACTH可能通过激活这些核团的神经元而发挥其中枢效应。

In present study, we demonstrated that μ opioid receptor and D1 dopamine receptor could form heteromeric complexes in membranes preparation from HEK293T cells transiently cotransfected with both receptors and from mice striatum.

在本工作中，我们通过免疫共沉淀和BRET法证明，HEK293T细胞上瞬时表达的μ阿片受体和D1多巴胺受体能形成异源二聚体，并证实μ阿片受体和D1多巴胺受体异源二聚体存在于小鼠纹状体中。

The expression of μ opiold recaptor of the knee joint synovium tissue in chronic inflammation was significantly up-regulated. It may play a partial role in the peripheral mechanism of morphine.

慢性滑膜炎时膝关节滑膜组织内阿片μ受体表达明显增加，这可以解释膝关节腔内使用阿片类药物缓解疼痛的作用机制。

However, opioid receptors are not expressed naturally in great abundance, they are relatively labile and frequently difficult to solubilize as monomers. The availability of their cDNAs makes them good candidates for overexpression in heterologous cells, which offers hope for the purification of membrane receptors for biochemical and structural studies.

在生物体内，阿片受体的含量很低，分离纯化过程中受体蛋白不稳定、易形成多聚体。cDNAs的克隆成功使阿片受体的异源高效表达成为可能，为研究阿片受体蛋白的生化特性和结构特征创造了条件。

We continue our discussion of the most commonly used analgesics in the management of pain, opioids.

我们继续讨论疼痛治疗中最常用的镇痛药—阿片药物。本周主要讨论阿片受体。

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。

In the normal brain and the body of some organs, the existence of endogenous opioid peptides and opioid receptor.

在正常人的脑内和体内一些器官，存在着内源性阿片肽和阿片受体。

In normal brain and body organs, there exist some endogenous opioid peptides and opioid receptors.

在正常人的脑内和体内一些器官，存在着内源性阿片肽和阿片受体。

In normal circumstances, endogenous opioid peptides in opioid receptors, adjust the person's mood and behavior.

在正常情况下，内源性阿片肽作用于阿片受体，调节着人的情绪和行为。

与阿片的相关的网络解释 [注：此内容来源于网络，仅供参考]

Opium：阿片

到公元前3世纪,古希腊和罗马的书籍中才对阿片有了详细的文字描述,当时阿片在古希腊享有广泛的大众性,"阿片"(opium)一词也是源于希腊词语"opion"(阿扁),意为"罂粟汁",希腊人将其用于癫痫、毒虫咬伤、忧郁症和各种瘟疫.

opium tincture：阿片酊

1.阿片制剂(opium preparation),如复方樟脑酊(tincture camphor compound)和阿片酊(opium tincture),为有效的止泻药而被广泛应用. 多用于较严重的非细菌感染性腹泻. 6.吸附药(adsorbants)和药用炭(medical charcoal),因其颗粒小,总面积大,

thebaic：阿片 阿片的

thebacone /醋氢可酮/ | thebaic /阿片/阿片的/ | thebaica /鸦片/

thebaic：阿片的

thebackthereversesidethewrongsideReverserearface 背面 | thebaic 阿片的 | thebaine 二甲基吗啡

opioid analgesics：阿片类镇痛药

因目前临床应用的镇痛药主要涉及阿片类镇痛系统,故也称为阿片类镇痛药(opioid analgesics). 纳洛酮(naloxone)为阿片受体阻断药, 它与阿片受体的亲和力比吗啡、内啡呔都强,但无内在活性,可对抗上述四种阿片受体亚型. 3.

opioid：阿片肽

1、阿片肽(opioid) 是最重要的内源性痛觉调节递质. 自1975年在脑内发现第一个内阿片肽-脑啡肽(ENK)以来,目前已发现了十几种内源性阿片肽,其中β-内啡肽镇痛作用最强,是吗啡的18~33倍,而甲硫脑啡肽作用极弱.

opioid receptor：阿片类受体

阿片类兴奋剂是一种通过附着在"阿片类受体(opioid receptor)"而产生作用的物质. "阿片类接受体"是一种特殊的蛋白质,分布于大脑、脊髓、胃肠道中. 当复方羟氢可待因附着在大脑和脊柱中的阿片类受体时,能有效阻断疼痛信息传送到大脑.

opioid peptide：阿片肽

几年后在哺乳动物脑中发现具有阿片样活性的肽类,阿片肽(opioid peptide). 阿片肽的大小相差颇大,从5个氨基酸的脑啡肽到31个氨基酸的β-内啡肽,但它们都有5个共同的氨基酸序列,即酪氨酸-甘氨酸-甘氨酸-苯丙氨酸-甲硫氨酸(或亮硫氨酸).

opioids：阿片类

(1)阿片类(opioids) 包括天然来源的阿片;从阿片中提取的有效成分如吗啡、可待因;将有效成分加工所得的产品如海洛因;也包括人工合成品如哌替啶(度冷丁)、美沙酮、芬太尼等.

opioids：阿片类药物

阿片类药物 opioids 38 | 阿片类药物的耐受和依赖 opioid toleranee and dependence 242 | 埃托菲 etorphine 40