可表达的

On the basis of the properties of central projection and orthographic projection, the differences of different rectification approaches based on orthographic projection are explained, and it is suggested that oblique-plane-rectified photograph can produce orthographic representation of flat terrain cover; differential rectification of RS imagery based on DEM can produce orthographic representation of waved terrain cover; and true orthographic rectification based on digital ground-object model can produce orthographic representation of single objects on ground.

根据中心投影和正射投影的特点，从理论上说明了不同正射投影纠正方法之间存在的差异，认为：基于透视变换的像片倾斜纠正可生成水平地表覆被的正射投影表达；基于DEM的正射影像微分纠正可生成起伏地表覆被的正射投影表达；基于数字地物模型的真正射纠正可生成独立地物的正射投影表达。

Producing PHAs,and then were orientationally inserted into a prokaryotic expression vector pBV220. By analyzing the bioactibity and function of their products, the biological function of phaA, phaB and phaC was confirmed. These have been done in our laboratory. To make better use of the three genes by plant bioreactor, two groups of different plant expression vectors that can be used to produce PHAs in different plants were constructed, and the transformation of PHA in Oxalis triangnlaris has been preliminarily reseached.The following is the main results:Three plant expression vectors pBI121-A,pBI121-B and ubquiting-C, which can be used to be transformed into Oxalis triangularis were respectively constructed by using the phaA, phaB and phaC.

菌株的亚克隆基因组片段中，分离出phaA、phaB和phaC三个基因片段，定向克隆至原核表达载体pBV220，通过对其生物活性与功能分析，确证了基因phaA、phaB和phaC的生物学功能；为了通过植物生物反应器对这三个基因进一步研究利用，本实验利用这三个基因构建了两组可用于不同植物生产PHA的真核表达载体，并对紫叶酢浆草进行PHA基因遗传转化的初步研究，获得主要结果如下：利用克隆的phaA、phaB、phaC三个基因分别构建了可用于转化紫叶酢浆草表达载体pBI121-A、pBI121-B、uBquiting-C；可用于玉米转化的种子特异性表达载体p7S-A、pBI121-S-B、uBquiting-C。

Results showed:(1) The airway responsiveness of smoke control group was higher than that of normal control group, the airway responsiveness of smoke + exercise group was lower than that of smoke control group;(2) Plasma level of cortisol determined immediately after exercise was higher than that determined before exercise, no significant difference occurs between that determined next day morning after all exercise finished in contrast to that determined before exercise;(3) HE staining showed, there was severe chronic pulmonary inflammatory response in smoke control group, which was reduced in the smoke + exercise group;(4) chronic cigarette smoke downregulated the protein and mRNA expression of BKca in smooth muscles of bronchi and bronchioli, exercise increased the mRNA expression of BKca;(5) chronic cigarette smoke downregulated the protein and mRNA expression of Kv1. 5 in smooth muscles of bronchi and bronchioli, exercise increased both the protein and mRNA expression of Kv1. 5 in contrast to smoke control group in bronchioli and did not effect the expression of Kv1. 5 in bronchi;(6) chronic cigarette smoke induced upregulation of FIZZ1/RELMα in bronchial smooth muscle cells, exercise decreased these effect.

结果：(1)吸烟对照组的气道反应性明显增高，吸烟加运动应激可明显降低大鼠的气道反应性；(2)吸烟运动组运动后血浆皮质醇浓度明显高于运动前，但全部运动结束后次日晨测定的血浆皮质醇浓度与运动前无明显差异；(3)HE染色显示，吸烟对照组肺组织出现明显的慢性炎症反应，吸烟加运动应激组比吸烟对照组炎症反应轻；(4)慢性吸烟可降低大鼠大气道和小气道BKca mRNA和蛋白表达，而吸烟加运动应激可使BKca mRNA表达上调，但对小气道的蛋白表达无影响；(5)慢性吸烟可降低大鼠大气道和小气道Kv1.5蛋白和mRNA表达，在小气道吸烟加运动应激可减轻这种作用，大气道则无作用；(6)吸烟使支气管平滑肌的FIZZ1/RELMα蛋白表达明显增强，而吸烟加运动组的RELMα蛋白及mRNA均明显减弱。

In the normal uterus, Cytokeratins immunolabelling were detected in glandular cell, luminal epithelial cell, Vimentin immunolabelling were detected in stromal cell and endoblastic cell; CK7 immunolabelling were not detected in any tissue of the yak utenus.

研究结果显示：未妊娠时，泛角蛋白在子宫内膜腺上皮细胞、腔上皮细胞内表达，波形蛋白在子宫内膜基质细胞内表达，平滑肌肌动蛋白在子宫平滑肌和血管平滑肌内表达，牦牛子宫任何部位均不表达角蛋白7；妊娠30天左右时，泛角蛋白在子宫内膜腺上皮细胞、子宫内膜腔上皮细胞、滋养层细胞、内胚层细胞和尿囊细胞内表达，波形蛋白在子宫内膜基质细胞和内胚层细胞内表达，平滑肌肌动蛋白在子宫平滑肌和血管平滑肌内表达，角蛋白7在尿囊细胞内表达，偶尔在腔上皮细胞的细胞核边缘表达；消化法进行原代培养时，组织经胶原酶消化并通过100目和400目筛网组合可以有效地分离原代子宫内膜基质细胞和子宫内膜腺上皮细胞；分离得到的子宫内膜基质细胞活率达90%以上，并可在体外传代7次以上；分离得到的子宫内膜腺上皮细胞活率可达85%以上，并可在体外传代5次以上；RPMI1640培养基最适合子宫内膜基质细胞和子宫内膜腺上皮细胞的生长，维持子宫内膜基质细胞正常生长的FBS添加量为20%，维持子宫内膜腺上皮细胞正常生长的胎牛血清添加量为30%。

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

A new eucaryotic expression system of recombinant PoIFN-γ was also constructed so that the denaturalization and refolding process is avoided. The target gene coding PoIFN-γ2 mature protein was subcloned into expression vector, transformed into Pichia pastoris, The His〓 Mut〓 phenotype transformants were screened, fermented in flasks and induced by 1％methanol. The expressed product in culture solution and sedimentation have antiviral activity on VSV and immunological activity proved by indirected immunofluorescence antibody and Dot blotting assay.

为了构建可对表达产物修饰、加工的真核表达系统，使表达产物具有自然干扰素的活性，无需变性、复性，我们将PoIFN-γ2成熟蛋白基因连接酵母整合表达载体，电转化毕赤酵母，筛选了His〓Mut〓表型转化子，摇瓶培养，1％甲醇诱导表达，培养上清和菌体裂解上清均有抗VSV病毒活性，经间接免疫荧光抗体检测和Dot blotting鉴定，重组酵母菌诱导表达产物具有免疫活性。

Outcome:(1) Acute ischemic damage may induce the expression of c-fos protein in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia. And the expression level of c-fos can be up-regulated by putting blood of 12 hand Jing Points. So we think that treated by this therapy can rise the irritability of brain to resist the development of ischemia and enhance the ability to plerosis.(2) Acute ischemic damage may induce the expression of HspVO in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia.

三 结果(1)急性缺血性脑损伤可快速诱导c-fos蛋白在皮层缺血区脑组织的表达，其表达有随缺血时间延长而逐渐增多的趋势，提示脑的缺血性损伤可应激性地增强神经细胞对缺血、缺氧的耐受和适应能力，而应用井穴放血的干预治疗可明显上调缺血区皮层脑组织c-fos的表达水平，进一步增强脑组织对抗缺血性损伤的应激能力，抵抗缺血性脑损害的进一步发展。

TUNEL method was used to detected the apoptosis in the artery. Results:①The MSC cocultured with VSMC expressed smooth muscle a-actin, calponin and CD31, no cells positive for calponin and CD31 were detected in the control group; and a lot of filaments were observed in the co-cultured MSC by electron microscopy.②We gain dual-stable expression of AT2R gene medicated by doxycycline regulatable system of mesenchymal stem cells.

单独培养及VSMC条件培养液培养的MSC仅SM-α-actin表达阳性；(2)Dox-on系统由四个质粒组成：调节质粒pUHD17-1 hyg，荧光报告质粒pUHC 13-3，筛选质粒pSV2neo以及含目的基因AT2R的应答质粒pUHD10-3/AT2R，以上质粒经鉴定均与其背景资料相符合，可用于实现目的基因片段在靶细胞中可调控表达研究；(3)本实验通过连续两个回合的转染及抗生素压力筛选，经Dox诱导表达后获取出低背景、高诱导表达AT2R基因的克隆。

Kangdai Ⅰ has protective function to the damaged neurons and astrocytes: Main results:(1) It has direct protective function to the damaged neurons. It can increase the activity and survival rate, decrease the mortality and the transudation rate of LDH in cultured medium and the strong positive cell count of NOS expression of injured neurons.(2) It has also directly protective function to the damaged astrocytes. It can increase the activity and survival rate and protein content in conditioned medium.(3) It can strengthen the ability of BDNF, GDNF, bFGF, HSP and IL-6expression in damaged astrocytes.(4) It can also strengthen obviously the expressions of NSE, bFGF-receptor and bc1-2, lower the expression of bax and caspase-3.(5) It can indirectly protect and restore the damaged neurons by astrocytes. Because the effect of ACMK (ACM interfered by Kangdai Ⅰ) is stronger than ACM+K (ACM associated with Kangdai Ⅰ).

抗呆Ⅰ号对受损的神经元和星形胶质细胞均具有保护作用：主要表现为：(1)对受损神经元具有直接的保护作用，可提高受损神经元的活性和存活率，降低细胞培养液LDH的漏出率、细胞死亡率和NOS染色强阳性细胞的表达量；(2)对受损的星形胶质细胞也有直接的保护作用，可提高其活性、存活率以及培养液蛋白质的含量；(3)能增强受损星形胶质细胞分泌BDNF、GDNF、bFGF、HSP和IL-6的能力；(4)可明显增强受损神经元对NSE、bFGF的受体和bc1-2的表达，降低受损神经元对bax和caspase-3的表达；(5)抗呆Ⅰ号可通过星形胶质细胞间接地保护和修复受损的神经元，因为在多数实验组中经抗呆Ⅰ号作用的ACM的作用远大于ACM与抗呆Ⅰ号联合应用的作用，统计学上具有显著性差异。

Results In 3T3-L1 adipocytes, isoproterenol at the concentration of 10 μmol/L reduced the adiponectin secretion and insulin at the concentration of 5 nmol/L could block the inhibitory effect of isoproterenol. In 313-Li adipocytes expressed myrAkt, adiponectin secretion decreased significantly, isoproerenol treatment increased adiponectin and insulin couldn't block the effect of isoproterenol.

结果 异丙肾上腺素可明显降低3T3-L1脂肪细胞脂联素的蛋白质表达，胰岛素可纠正这一变化；表达myrAkt的3T3-L1脂肪细胞中脂联素明显减少，异丙肾上腺素可增加脂联素蛋白的表达，胰岛素不能纠正这一变化。

Lugalbanda was a god and shepherd king of Uruk where he was worshipped for over a thousand years.

Lugalbanda 是神和被崇拜了一千年多 Uruk古埃及喜克索王朝国王。

I am coming just now,' and went on perfuming himself with Hunut, then he came and sat.

我来只是现在，'歼灭战perfuming自己与胡努特，那麼，他来到和SAT 。