抑制剂

The matrix metalloproteinases are a family of functionally related zinc-containing enzymes that denature and degrade fibrillar collagens and other components of ECM.

基质金属蛋白酶组织抑制剂-1(tissue inhibitor of metalloproteinase-1，TIMP-1)是MMPs的内源性组织抑制剂，是体内调节MMPs活性的重要物质。

It was expected that this work could provide some helpful insights into the nature of mutational influences and aid design of better inhibitors in the future.

研究结果有助于更好地理解变异对抑制剂和HIV-1 PR结合模式的影响，并可以用来帮助设计更高效的PR抑制剂。

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 calmodulin antagonists (calmidazolium, W7agarose) and anticalmodulin serum had inhibitory effect on the extracellular reduction of ferricyanide with their concentration that yielded 50% inhibition were 1.5 μmol/L, 10 μmol/L and 10 mg/L respectively.

结果表明，大分子的CaM抑制剂W7agarose、小分子抑制剂calmidazolium及CaM的抗血清对跨质膜铁氰化钾的还原均有不同程度的抑制作用，半抑制浓度分别为10μmol／L、1.5μmol／L和10mg／L。

Pretreatment of HUVEC with Ras inhibitor or a ROCK (a kinase associated with RhoA for transducing RhoA signaling) inhibitor, Y27632, abolished the FOH or GGOH induced prevention effect on the TB-induced migration inhibition, respectively.

另外，以Ras抑制剂或ROCK(藉由与RhoA接触而传递相关讯息的下游分子)抑制剂(Y27632)进行预处理则能使原本FOH或GGOH对於TB作用的预防效果消失。

These small molecules include FTY720, a sphingosine phosphate-receptor modulator, FK778, an inhibitor of pyrimidine synthesis, CP-690550, a JAK3 inhibitor, and AEB-071, a protein kinase C inhibitor.

这些小分子包括FTY720，一种神经鞘氨醇磷酸盐受体调节剂；FK778，一种嘧啶合成抑制剂；CP-690550，一种JAK3抑制剂及AEB-071，一种蛋白激酶C抑制剂。

However, dexamethasooe did not seem to affect the sustained current and the sustained component of the biphasic current induced by ATP. The in hibitory effect of dexamethasonc on ATP induced currents was blocked by glucocorticoid receptor antagonist RU38486 (10μmol/L) and protein kinase A inhibitor H-89 (10μmol/L), but not by G protein inhibitor GDP-β-S (0.2mmol/L) and protein kinase C inhibitor chelerythrine chloride (10μmol/L).

地塞米松对ATP激活电流的快速抑制作用可被糖皮质激素受体拮抗剂RU38486(10μmol/L)、蛋白激酶A抑制剂H-89(10μmol/L)阻断，而G蛋白激活抑制剂GDP-β-S(0.2mmol/L)、蛋白激酶C抑制剂Chelerythrine chloride(10μmol/L)对地塞米松的快速抑制作用无明显影响。

Subcordiformis in Huanghai Sea near Dalian, it can be able to evolve H〓 photosynthetically. Comparing with Chlamydomonas reinhardtii in our lab, the H〓 productivity is same. By the elementary macro regulation of H〓 production with 2, 5-dibromo-3-methyl-6-isopropyl-p-benzoquinone , N, N'-dicyclohexylcarbodiimide , 3-(3, 4-dichlorophenyl)-1, 1-dimethylurea , sodium dithionate, sulfur-deprivation and cell immobilization, the results show that DCCD, immobilization and sulfur-deprivation has a positive effects on the H〓 production.

利用DCCD（质子泵抑制剂N，N'-dicyclohexylcarbodiimide）、DBMIB（光合电子传递抑制剂2，5-dibromo-3-methyl-6-isopropyl-p-benzoquinone）、DCMU[PSⅡ光合放氧抑制剂3-（3，4-dichlorophenyl）-1，1-dimethylurea]、连二亚硫酸钠、无硫调控及固定化扁藻等手段，对该扁藻产氢进行初步的宏观调控，发现DCCD的加入、扁藻的固定化和无硫调控对产氢均有正效应，其中无硫调控使扁藻产氢时间延长，总产氢量提高了近10倍。

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。

Finally, according to market conditions and market products this article paper analyzes the trends in the development of camera technology, and designs a color night vision camera.

最后根据市场情况和市面上产品的情况分析了摄像机技术的发展趋势，并设计了一款彩色夜视摄像机。

Only person height weeds and the fierce looks stone idles were there.

只有半人深的荒草和龇牙咧嘴的神像。