普遍性的、全身性的

指某种脑电活动如3Hz的棘慢波暴发是全脑区出现的，可以说是普遍性分布的。指癫痫发作不是局限于某个肢体的局部性发作，而是全身都在发作如强直阵挛发作，可以说是全身性发作。     

您的云是什么样的

如果要在下图的天空里描绘云朵，您会描绘出什么样的云？请从下面的选项中选择。 这是根据图画而诊断人的性格的心理测验。在所描绘的画中可以反映人的性格。尤其是一些像云一样的暧昧不明的物体，更能凸显人的个性。     

高血压的药物基因组学的研究进展

本文综述了近几年来关于原发性高血压治疗常用的6种主要降压药物(利尿剂、β肾上腺素能受体阻滞剂、钙拮抗剂、血管紧张素转化酶(ACE)抑制剂、血管紧张素Ⅱ受体拮抗剂和α肾上腺素能受体阻滞剂)的作用机制、代谢途径和药物基因组学候选基因的研究进展,以期获得原发性高血压药物基因组学候选基因相关信息。为原发性高血压的预防和个体化治疗提供参考依据。     

高血压的药物基因组学的研究进展

本文综述了近几年来关于原发性高血压治疗常用的6种主要降压药物(利尿剂、β肾上腺素能受体阻滞剂、钙拮抗剂、血管紧张素转化酶(ACE)抑制剂、血管紧张素Ⅱ受体拮抗剂和α肾上腺素能受体阻滞剂)的作用机制、代谢途径和药物基因组学候选基因的研究进展，以期获得原发性高血压药物基因组学候选基因相关信息。为原发性高血压的预防和个体化治疗提供参考依据。     

您的云是什么样的

<正>如果要在下图的天空里描绘云朵,您会描绘出什么样的云?请从下面的选项中选择。这是根据图画而诊断人的性格的心理测验。在所描绘的画中可以反映人的性格。尤其是一些像云一样的暧昧不明的物体,更能凸显人的个性。     

教学用的柔软的气管模型的建造

<正> 作者描述了制造柔软、强韧的狗气管模型方法,用压缩空气使狗肺在充气下干燥,之后灌硅酮填充剂,待此复合物干燥后,用氢氧化钠(NAOH)腐蚀肺组织。最后是一个凹凸不平的、柔软的和在解剖学上适合     

我的阳光灿烂的日子

我的日子阳光灿烂．不是因为给我一点阳光我就觉得灿烂，而是因为灿烂，所以我觉得阳光。     

适合的就是好的

我习惯于中学时有老师指导的学习方式，字习成绩优秀，而且顺利地考上了重点高中。可是进了高中，我才发现自己不但没有优势，而且由于没有养成好的学习习惯，甚至根本不会学习（也许说不会自己学习更确切）。由于住校，也不能及时地得到父母的帮助，这一问题显得更加突出。我虽然作过各种努力，但始终效果不佳，学习成绩也受到影响。眼看离高考的时间越来越近，我真的非常焦急。恳求您教我一个在短时间内能见效的、好的学习方法!     

天然的或人工合成的致癌突变剂的抑制剂

过去几十年内人类恶性肿物的发病率普遍有所增加,这与以下几种因素有关:1)检测恶性肿物的诊断筛选方法得到改进,2)发现并发展了治疗传染性和其他疾病的新的更有效的抗菌素以及化疗药物,致使年青人的死亡率降低,因此,平均寿命有所延长,从而使老年人口中癌的发生率上升,3)工业的和其他致癌物的环境污染增加,诸如新工厂、汽车和化学实验室等。至今至少已经证实有一千种以上致癌化合物能有效地诱导人类肿瘤的发生,特别是居住在工业区的人群。     

钛的氩弧焊试件的应力腐蚀的实验研究

纯钛的氩弧焊试件承受 2 6 1MPa ,37℃人工唾液 3个月的应力腐蚀试验后 ,力学性能无明显改变 (P >0 0 5 ) ,表面无颜色改变和显微裂纹 ,表明其具有好的抗应力腐蚀性能。     

肝细胞增殖因子促进受损肝细胞增殖的可能机制

目的： 探讨肝细胞增殖因子（ALR）促进受损肝细胞增殖的可能机制。方法: 采用细胞增殖试验（MTT法）观察经ALR刺激的大鼠肝枯否细胞(KC)的条件培养液(KCCM+)对受损肝细胞增殖的影响，同时用免疫组织化学方法检测正常大鼠肝脏组织中ALR的分布、大鼠枯否细胞膜表面结合的ALR以及ALR对枯否细胞IL-6表达的影响。结果: 受损肝细胞经枯否细胞条件培养液刺激后增殖明显。正常大鼠肝细胞内可表达合成ALR，枯否细胞膜表面可见ALR免疫反应颗粒，经ALR刺激后枯否细胞IL-6免疫反应信号增强。结论: ALR可能通过首先刺激枯否细胞，从而促进受损肝细胞增殖。     

Role of estrogens as promoters of hepatic neoplasia

The administration of estrogens to humans has been associated with the development of benign and possibly malignant hepatocellular neoplasms. This study was designed to investigate the mechanism of this association. We present a rat model that demonstrates that stilbestrol (DES) and ethinyl estradiol promote the development of hepatic neoplasms in rats previously initiated with diethylnitrosamine (DEN). Eighty male and 12 female Fischer-344 rats were given a single intraperitoneal injection of either DEN (200 mg. per kg. of body weight) or saline. Beginning 4 weeks after injection, the rats were given an estrogen or corn oil twice weekly for up to 50 weeks. Treatments were stopped at the time of sacrifice or 11 to 29 weeks prior to sacrifice. Estrogen treatments included high dose DES (5 mg. per dose), low dose DES (0.5 mg. per dose), and ethinyl estradiol (0.2 mg. per dose). Male and female rats given both DEN and high dose DES developed grossly visible hepatic hyperplastic nodules (mean, 9.1 per liver) after 20 weeks of DES. Nodules also developed if the onset of DES treatment was delayed until 28 weeks after initiation. Rats given DEN alone or DES alone did not develop nodules after 20 weeks. Microscopic hyperplastic foci also developed in rats given DEN plus DES, DES alone, and DEN alone. The foci in rats given DES alone were largely reversible on cessation of estrogen therapy. Mitotic activity in foci and nodules was prominent during estrogen therapy but declined markedly after cessation of therapy. Similar promoting activity of ethinyl estradiol was observed. Low dose DES was not effective in promoting tumor formation. The data indicate that estrogens promote hepatic neoplasia, perhaps by increasing hepatocyte mitotic activity and thereby facilitating the evolution of previously initiated cells into neoplastic clones. Comparison with human disease should be made with caution, especially because the estrogenic dose administered was approximately 200-fold the usual contraceptive dose in humans. However, the analogy between this model and the development of human oral contraceptive-associated hepatic tumors is evident. It is possible that some women have latent "initiated" cells that divide faster than the surrounding hepatocytes in response to estrogens.     

Immunohistochemical detection of estrogen receptor �� in alveolar bone cells of estradiol-treated female rats: possible direct action of estrogen on osteoclast life span

The role of estrogen in bone resorption has been specifically related to the effect of estrogen on the signalling pathway that inhibits the formation of osteoclasts. However, osteoclast apoptosis and a significant reduction in the number of these cells have been observed in the alveolar bone of female rats treated with estradiol. In the present study, the expression of estrogen receptor β (ERβ) in the cells of alveolar bone was evaluated in estradiol‐treated and ‐untreated female rats. In order to test the possible direct action of estrogen on osteoclasts, the relationship between apoptosis and ERβ expression in these cells was also analysed. The animals received estradiol for 14 days and the alveolar bone fragments were embedded in paraffin for the quantification of tartrate‐resistant acid phosphatase‐positive osteoclasts. The expression of ERβ and apoptosis in the osteoclasts were evaluated by ERβ immunohistochemistry and Terminal deoxynucleotidyl transferase‐mediated dUTP Nick‐End Labelling (TUNEL) methods, respectively. To confirm osteoclast death by apoptosis, these cells were analysed under transmission electron microscopy. Some osteoclasts from estradiol‐treated animals were found to be undergoing apoptosis and the number of tartrate‐resistant acid phosphatase‐positive osteoclasts was significantly reduced. ERβ immunolabelling was observed in the cytoplasm and nuclei of active osteoblasts, osteocytes and osteoclasts in both groups, suggesting a direct participation of estrogen on alveolar bone cells. However, following estradiol treatment, a strong ERβ immunolabelling was often observed in the TUNEL‐positive osteoclasts. Therefore, these results indicate that, in addition to the other signalling pathway, the reduction of alveolar bone resorption is also related to a direct action of estrogen on osteoclasts, promoting apoptosis in these cells, via ERβ.     

大鼠实验性隐睾对睾丸间质细胞的影响

目的 探讨大鼠实验性隐睾丸间质细胞数量、形态及相关功能的影响.方法 采用手术诱导方法制作大鼠(6月龄)双侧隐睾模型(每组6只),分别于术后第3天、7天、20天和28天取左侧睾丸入Bouin液固定,假手术组作为对照组.应用体视学方法检测睾丸间质细胞的数量、形态变化;应用免疫组织化学检测细胞分裂周期蛋白25A(CDC25A...     

雌激素受体α和TrkA在基底前脑的分布与共存

基底前脑为神经营养因子和雌激素作用的靶区之一。为了在受体水平探讨这些配体是否作用于正在发育和成年大鼠的基底前脑同一神经元 ,本文采用免疫组织化学双重反应方法观察了雌性大鼠雌激素受体α和酪氨酸激酶 A在基底前脑的分布与共存。用小鼠抗雌激素受体和兔抗酪氨酸激酶 A分别孵育切片 ,ABC法显示前者的反应产物主要位于胞核内 ,蓝黑色 ,呈点状 ;后者位于胞质和突起内 ,呈棕色。结果表明 :两者都分布于基底前脑神经元。在双重免疫组织化学反应条件下可见三种细胞 :雌激素受体阳性细胞 ,酪氨酸激酶 A阳性细胞和双重反应阳性细胞 ,双重反应阳性细胞所占的比例因部位而不同。雌激素受体和酪氨酸激酶 A共存提示它们的配体可通过共存于基底前脑同一神经细胞上的相应受体而作用于同一神经元 ,协同地调节特异的基因或者基因网络的表达 ,从而影响神经元的存活、分化、成熟、再生和可塑性     

Nuclear localization of estrogen receptor-immunoreactivity in the preoptic area of female rats and its reduction by intraventricular colchicine treatment.

The subcellular localization of estrogen receptor (ER) was investigated in the preoptic area of ovariectomized female rats by electron microscopic immunohistochemistry, using a monoclonal antibody to ER. ER-immunoreactivity was localized in the nuclei of neurons of the periventricular preoptic nucleus (Pe) and the medial preoptic area (MPA). ER-immunoreactivity had a speckled pattern in the nucleus, but was not observed in the nucleolus or cytoplasm. After intraventricular colchicine treatment, ER-immunoreactivity within the nucleus was reduced drastically in neurons of the Pe and the MPA. The possible mechanism by which colchicine alters ER-immunoreactivity is mentioned.     

左旋18-甲基炔诺酮对大鼠雌激素水平及下丘脑雌激素受体阳性细胞的影响

目的:观察左旋18-甲基炔诺酮(LNG)对大鼠雌激素(E)水平及下丘脑内雌激素受体(ER)阳性细胞的影响。方法:正常雌性SD大鼠分为给药对照组、给药组、停药对照组、停药组,应用免疫组织化学方法显示下丘脑ER阳性细胞并检测血清E浓度。结果:给药组较给药对照组E浓度下降,弓状核(Arc)、下丘脑腹内侧核(VMH)内ER阳性细胞的数量减少、光密度下降。停药后基本恢复正常。结论:长期LNG作用导致给药大鼠血清E水平下降;长期LNG作用引起大鼠下丘脑ER数量减少、活性减低,推测ER可能参与影响促性腺激素释放激素的分泌;停药后ER的形态学变化恢复正常,所以LNG的作用基本上是可逆的。     

Hepatocyte modulation of Kupffer cell prostaglandin E2 production in vitro

It is likely that dynamic interactions between hepatocytes and Kupffer cells contribute to the responses of these cell types both under normal conditions and during sepsis. In this study, we examined the influences of hepatocytes on the concentration of the inflammatory mediator PGE2 in Kupffer cell cultures. Evidence to suggest that cultured rat hepatocytes both metabolize PGE2 and produce a substance that promotes LPS-stimulated Kupffer cell PGE2 biosynthesis include the following: 1) PGE2 levels in Kupffer cell: hepatocyte coculture were lower than the levels in Kupffer cell cultures early after LPS stimulation; 2) 36 h after LPS, coculture PGE2 levels exceeded the levels in Kupffer cell cultures despite the demonstrated capacity for hepatocytes to metabolize PGE2; 3) a transferable, non-dialyzable, and heat-unstable factor in hepatocyte supernatant promoted PGE2 production when added to Kupffer cells with LPS or after LPS; 4) there was no increased PGE2 synthesis when the hepatocyte supernatant was added without LPS or if hepatocyte supernatant was preincubated with the Kupffer cells for 6 or 18 h before LPS administration; 5) there was an inability of the hepatocyte factor to promote PGE2 production in response to other macrophage-activating agents, including calcium ionophore A23187 or phorphol myristate acetate; and 6) there was no increased cell replication or protein synthesis in the Kupffer cell cultures following hepatocyte supernatant incubation. The increased Kupffer cell PGE2 production by the hepatocyte supernatant was not due to contamination of the hepatocyte supernatant by endotoxin or PGE2. These in vitro results raise the possibility that hepatocytes have the capacity to modulate local PGE2 levels by two distinct mechanisms. Hepatocytes can metabolize PGE2 as well as release factor(s) which promote LPS-induced PGE2 production by Kupffer cells.     

The role of Kupffer cells in liver regeneration

The liver has a remarkable proliferative capacity after a partial hepatectomy. Previous studies have indicated that Kupffer cells have the potential to exert both stimulatory and inhibitory influences on hepatocyte proliferation. To elucidate the role of Kupffer cells in liver regeneration, mice were selectively depleted of Kupffer cells by injection of liposome-encapsulated dichloromethylene diphosphonate (lipo-MDP) at day 3 after a two-thirds hepatectomy. Results showed that liver regeneration was delayed after Kupffer cell-depletion. In control mice, hepatocyte growth factor (HGF) mRNA expressions were enhanced during liver regeneration and expressions of HGF were localized in fat-storing cells (Ito cells). In Kupffer cell-depleted mice, the number of HGF-expressing cells decreased in the regenerating liver, and expressions of HGF and its receptor (c-met) as well as other growth factors/cytokines were less prominent than in control mice. In contrast, expressions of TNF-alpha, another potent cytokine involved in liver regeneration, did not differ between Kupffer cell-depleted and control mice during the regeneration. Administration of TNF-alpha antibody did not reduce the expression of HGF or liver regeneration. These findings imply that Kupffer cells play a stimulatory role in liver regeneration by enhancing HGF expression via TNF-alpha-non-mediated mechanisms.