受体

Our results demonstrate: The structures of the organs are normal, and the shapes of cells are clearly visible. There are lots of positive brown granules in Chief cells and Parietal cells in abomasum as well as the mucosa epithelial cells and gland cells of duodenum. Three bands with a molecular mass close to 120KDa、110KD and 98KDa were identified by Western Blot. The Ob-R levels of 120KDa in abomasum were significantly higher than that of in small intestine. The levels of 110KDa were similar in the two organs. The expression of 98KDa Ob-R was weak.

HE染色结果显示，各组织结构正常，细胞形态清晰可见；免疫组织化学SABC染色显示，在皱胃胃体部固有层胃底腺的主细胞和壁细胞及十二指肠黏膜上皮细胞和固有层肠腺的柱状细胞中均可见大小数量不等的棕黄色颗粒；western Blot 实验发现，在胃和小肠均检测到120KDa、110KDa和98KDa三条带。120KDa长型瘦素受体蛋白在胃中表达量显著高于小肠中的表达；110KDa的短型瘦素受体蛋白，在小肠和皱胃中表达量接近。98KDa短型受体蛋白在胃和小肠表达均较弱。

Immunofluorescence confirmed that sweat glands in normal mice did not present gamma-aminobutyric acid receptor subtype GABAA andα-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainic acid subtype of glutamate receptor. Mature mice with reactive sweat glands that declined more than 25% compared to baseline were defined as anhidrotic mice.

免疫组织荧光染色未发现在正常小鼠皮肤组织及汗腺的分泌细胞存在γ-氨基丁酸A型(gamma-aminobutyric acid，GABAA)受体α1亚单位、谷氨酸受体亚型α-氨基羟甲基恶唑丙酸(α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid ， AMPA )GluR1/2/3/4亚单位和海人酸(kainic acid，KA)受体GluR5/6/7亚单位的表达。

Immunofluorescence confirmed that sweat glands in normal mice did not present gamma-aminobutyric acid receptor subtype GABAA andα-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainic acid subtype of glutamate receptor.Mature mice with reactive sweat glands that declined more than 25% compared to baseline were defined as anhidrotic mice.

免疫组织荧光染色未发现在正常小鼠皮肤组织及汗腺的分泌细胞存在γ-氨基丁酸A型(gamma-aminobutyric acid，GABAA)受体α1亚单位、谷氨酸受体亚型α-氨基羟甲基恶唑丙酸α-amino(来源：Ad1d1BC论文网www.abclunwen.com-3-hydroxy-5-methylisoxazole-4-propionic acid ， AMPA GluR1/2/3/4亚单位和海人酸(kainic acid，KA)受体GluR5/6/7亚单位的表达。

There was an obvious increase of insulin receptor gene and protein in the cerebral ischemia reperfusion tissues in rats. The positive cells such as neuron, neuroglia cells, vascular endothelium cells possibly participated in regulating the processes of energy metabolism of cells and neovascularization. It implied that the high expressions of insulin receptors in vascular endothelium cells in ischemic zones possibly participated in regulating the pathophysiological changes of the blood vessels in ischemic zones; The higher expressions of insulin receptors in different cells were possibly one of the self-protective machanisms in which the ischemic tissues confront the anoxemia injury.

脑缺血再灌注大鼠脑组织胰岛素受体基因和蛋白水平表达增加；半暗带区神经元、部分神经胶质细胞及血管内皮细胞等阳染细胞可能参与脑缺血后组织细胞的能量代谢、促新生细胞形成等病理生理调节过程；胰岛素受体在缺血区血管内皮细胞高表达提示其可能在缺血区血管的病理生理变化中起某种调节作用；胰岛素受体在不同细胞中表达增高可能是缺血脑组织对抗缺血缺氧损伤的自身保护机制之一。

The possible role of cross-inhibition between GABA_aRs and GlyRs in the CNS I then examined synaptical coupled cultured neurons from the IC to test for the possible role of this cross-talk during GABA_AR-mediated neurotransmission.

此外，通过转染甘氨酸受体α亚基在培养的下丘神经元上提高甘氨酸受体表达，结果发现甘氨酸受体和GABA_A受体所引起的电流比值显著性的增加，并且交互抑制的模式也从对称性的转变为非对称性的或单向的交互抑制。

After binding with ligands, the RTKs would dimerize, simultaneously autophosphorylated and activated and then trigger the downstream signaling pathway.

大量工作表明，配体与受体结合，引起受体的二聚化并同时激活受体后，受体可结合大量的信号蛋白分子，如接头蛋白、入坞蛋白或各种调节蛋白等。

First, the significant of co-factor InsP6 and center water in the mechanism of auxins are explored by docking; second, the experiments that compared with the docking rusults of two situations involving fully rigid and selective flexible of active residue of the receptor TIR1 illuminate that selective flexibility docking by AutoDock4 reports more rational results, so that, AutoDock4 dockings are implemented with TIR1-Auxins; third, AutoDock4 docking by TIR1-Auxins-Aux/IAA illuminates that auxin as a molecular glue enhances the interaction between TIR1 receptor and Aux/IAA substrate by the weak interactions, such as hydrogen bond and hydrophobic interaction, furthermore, the weak interactions between receptor protein and ligands greatly influence on auxin activity of auxin ligands.

首先， 通过分子对接计算研究辅酶InsP6以及中心水分子在生长素反应中的重要作用；其次，比较受体大分子完全刚性以及活性残基部分柔性的两种情况下的分子对接结果，说明AutoDock4实现了受体分子活性残基的部分柔性而使对接结果更加合理，进而使用AutoDock4方法对TIR1-Auxins体系进行对接计算；最后，对TIR1-Auxins-Aux/IAA体系进行分子对接计算，结果表明，生长素配体分子作为&分子胶水&直接与受体大分子TIR1以及底物多肽Aux/IAA形成强的弱相互作用，如氢键作用、疏水相互作用，促进了受体TIR1与Aux/IAA底物之间的结合，进而说明氢键作用和疏水相互作用等弱相互作用对于生长素分子的活性具有很大的影响。

Aim:(1) The purpose of this study is to examine whether protein tyrosine kinase and AMPA receptor in the nucleus tractus solitarius and nucleus ambiguus were involved in the regulation of normoxia and hypoxia respiratory response by microinjection of PTK inhibitor and non-NMDA receptor antagonist;(2) To observe the change of number of phosphotyrosine immunopositive neurons in NTS and NA before and after hypoxia using immunohistochemical methods and whether tyrosine phosphorylation and GluR1 in postsynaptic membrane co-localize in NTS and NA neurons.

目的：(1)观察向家兔脑干孤束核或疑核内微量注射酪氨酸蛋白激酶阻断剂和谷氨酸AMPA受体阻断剂对常氧呼吸和低氧呼吸反应的影响，探讨PTK和AMPA受体在低氧呼吸反应中的作用。(2)观察低氧通气后NTS和NA磷酸化酪氨酸免疫阳性神经元的数量变化；观察磷酸化酪氨酸和AMPA受体亚单位GluR1在突触后膜共存的情况，推测在低氧呼吸反应中AMPA受体和PTK信号转导途径的关系。

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。

Which play a major role in the pathological changes of restenosis after angioplasty But AT2 receptor is only expressed abundantly in the fetal vasculature with rapid decline after birth and the level of re-expression in the adult vasculature after injury is very low So there are little understanding about the actions of AT2 receptor in vascular diseases, especially in the restenosis after injury.

在寻致或加重VSMC增殖和迁移诸多因素中，血管紧张素Ⅱ所介导的生物学作用是其中重要的因素之一。AngⅡ具有多种生物学作用，其作用的多样性是通过其受体的多样性介导的，目前已确定的AngⅡ受体至少有两型，即AngⅡ 1型受体(AT1R)和AngⅡ 2型受体(AT2R)。

In the United States, chronic alcoholism and hepatitis C are the most common ones.

在美国，慢性酒精中毒，肝炎是最常见的。

If you have any questions, you can contact me anytime.

如果有任何问题，你可以随时联系我。