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The bodies have much greater potential to regulate spermatogonial stem cell proliferation and differentiation. The dosage of GFRα1 mRNA produced by undifferential spermatogonial cells regulates the signal transduction of glial cell-derived neurotrophic factor so as to regulates the direction of spermato gonial stem cells: at a low level, spermatogonoial stem cell favors differentiation; at a high level, spermatogonial stem cell favors self-proliferation.

GFRαl在小鼠生精恢复过程中以剂量相关性调控著胶质细胞源性神经营养因数资讯传人，从而调控著精原干细胞的去向：高剂量时诱导其增殖，低剂量时诱导其分化。

These cancer cells might histogenetically be related to the transitional or metaplastic epithelium of prostate according to morphological analysis,(2) Mucinous adenocarcinoma, Xanthomatous carcinoma, ductal carcinoma, medullary carcinoma, endometrioid carcinoma, papillary carcinoma and signet-ring cell carcinoma were positive for PSA and 35βH11, these carcinomas might histogenetically be related to prostatic secretory epithelium,(3) Prostatic carcinoid showed positive to PSA, 35βH11, NSE and CgA, corresponded with endocrine cell originator,(4) Small cell carcinoma were negative for PSA, 35βH11, NSE and CgA, whether or not it originates from endocrine cells, storage cells or basal cell of prostate had yet to be proved,(5) 34βE12 marking was negative in cancerous areas of 27 cases, and the basal cells were absent in PPTC.

从形态分析，这两种癌可能同源于移行上皮或化生上皮：（2）粘液腺癌、黄色瘤样癌、导管癌、髓样癌、宫内膜样癌、乳头状癌及印戒细胞癌均显PSA及35βH11阳性，提示这几种癌可能来源于分泌上皮，（3）类癌对PSA、35βH11、NSE及CgA均显阳性，符合内分泌细胞来源，（4）小细胞癌无PSA、NSE及CgA表达，对c-erbB-2及35βH11显阳性，是否来源于前列腺内分泌细胞、储备细胞或基细胞有待证实，（5）27例癌区均无34βE12表达，提示PPTC中基细胞缺失。

Comparative studies of electroactive components and voltammetric behaviors different between the MCF-7 cell without estrogen and the MCF-7 cell with estrogen showed that the concentration of the guanine and xanthine bases in the cytoplasm decreased, which resulted in the decrease of secretion ability of the MCF-7 cell without estrogen decreased, and these result in the decreasing of the voltammetric response of the cells, impling that the cell vaibility decreases.

结果发现，去激素MCF-7细胞质中的黄嘌呤和鸟嘌呤浓度降低，使细胞分泌黄嘌呤和鸟嘌呤能力降低，导致细胞和细胞质的伏安信号减弱，说明去激素MCF-7细胞的活性下降；研究了标准雌激素雌二醇、环境雌激素壬基酚和双酚A对去激素培养的MCF-7细胞增殖的影响，发现其均存在剂量-效应关系和时间-效应关系，并且雌激素效应由大到小的顺序为：雌二醇＞壬基酚＞双酚A；同时使用3-(4，5-Dimethylthiazol-2-yl)-2，5-diphenyltetrazolium bromide法验证了电化学法评价雌激素效应的可靠性。

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。

In the second part of our research, YC-1, an indazole derivative, displayed impressive selective toxicity against the human lung squamous carcinoma cell line NCI-H226 and human kidney tumor cell lines RXF-631L by a panel of 39 human cancer cell lines (JFCR39) screening. Therefore, the molecular mechanism by which YC-1 affects NCI-H226 cell growth was studied.

在本论文的第二部份中，吲唑类化合物YC-1经利用日本JFCR39癌细胞株之抗癌活性筛选后发现，YC-1对於人类肺鳞状上皮细胞癌细胞NCI-H226以及人类肾癌细胞RXF-631L具有高度的抑制选择性，於是我们选择NCI-H226细胞株做为YC-1对抗肺癌之抗癌机制探讨模式细胞。

The distribution of PTA1 molecule on NK cell, NK cell lines and NK cell clone was detected by indirected immunofluorescence staining and FCM analysis. The results showed that PTA1 expression rate on activated NK cell in MLC was above 60%.

结果证明这种方法能够稳定获得NK细胞克隆，应用流式细胞仪检测获得的一株NK细胞克隆表型为 CD56CD3－。

Microtubules and their textural composite hydrate system, nuclear envelope inside the cell, the places of plasma membrane infolding and cell junction and cell adhesion outside the cell possess lots of nano-scale (100-103 nm) narrow spaces.

在细胞内部的微管及其织构复合水化体系、核膜以及在细胞外部的质膜内褶和细胞连接粘连之处都可以发现许多纳米尺度(100~103 nm)缝隙空间。

After 6 to 7 days of culture, Eleven ES cell lines were selected and explanted. At last we obtained 4,3,4 and 3 ES cell lines separately. One of the B6C3F_1×B6D2F_1 ES cell lines was selected to future study its competent for germline transmission.We founded the ES cell line has normal karyotype on the chromosome analyse.In teratoma experiment by injected ESCs into C57 mices inguen, we gained teratoma contained cells come from all three embryonic germ layers.

选择一株具有高度杂合背景的B6C3F_1×B6D2F_1 ES细胞系进行核型分析、畸胎瘤实验后与ICR品系2n胚胎构建嵌合体并得到具有生殖系传递能力的嵌合体小鼠，证明此细胞系具有生殖系嵌合能力。

ResultsThe glandular cell in the endometrial implant after therapy with middle or high-dose of (10,15 gkg-1d-1) XiaoChaiHu Decoction showed characteristic features of apoptosis which displayed by the cell decreased in size, karyopyknosis , cytoplasmic and nuclear chromatin condensation , density increased and a lot of apoptotic bodies among cell. Whereas some stromal cell displayed degeneration and necrosis. The protein expression of Fas and Caspase-3 in endometriotic tissue of XiaoChaiHu Decoction group was higher than that in the endometrium.

结果中、高剂量小柴胡汤（10，15 gkg-1d-1）治疗后，异位内膜有较多腺上皮细胞出现凋亡的特征，表现为细胞体积变小，核固缩，胞浆和核染色质凝集，密度增高，细胞间凋亡小体，同时间质细胞中可见一些坏死细胞；异位内膜Fas蛋白、Caspase-3蛋白的表达水平明显高于其在位内膜。

And the long axis of simple pit Varied along with CMfs orientation of each secondary wall.This paper proposed a structure model of Phyllostachys pubescens cell wall,based on the results of CMfs deposition and thickness of each secondary wall.Secondly, it was a multilamellate structure of parenchyma cell wall,but its thin and thick lamellate was not evident.CMfs orientation on primary wall of parenchyma cell was perpendicular to cell axis.

纤维的细胞壁为典型的薄厚层相间的同心圆多层结构，初生壁CMfs排列方向与细胞轴向垂直90°次生壁中厚层的CMfs均以接近平行的小角度(0～5°沉积；薄层一般以大角度沉积，且薄层的CMfs角度由壁外侧向细胞腔里逐渐增加，直到完全垂直。

You can snipe the second and third union leaders from this position.

您可以鹬第二和第三工会领袖从这一立场出发。

Aiming at the currently shortage of XML streams quality detecting, this paper proposes a new forecasting method of XML streams quality by least squares support vector machines, which is used the method of XML keys' vector matrix as windows, and vector product wavelet transform to multilevel decompose and refactor the XML streams series, that can fulfill real-time checking demand of XML quality, and ensure constraint, consist- ency and integrality. For even more adapting net load, it proposes a control strategy by weight and adaptive adjustment to ensure XML streams quality.

针对当前XML数据流质量检测存在的不足，提出构建XML键的矢量矩阵作为窗口，利用矢量积小波变换多级分解与重构XML数据流，再结合最小二乘支持向量机对XML数据流质量进行预测的一种方法，满足XML数据流质量重构时实时检测的要求，保证XML数据的约束性、一致性与完整性；为了更好的适应网络负载，采取加权与自适应窗口调整等调度策略充分保证XML数据流的质量检测。