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1.
Background Ginsenoside Rg3, the main component isolated from ginseng, inhibits some kinds of tumour growth and angiogenesis. The combination of low dose chemotherapy and antiangiogenesis inhibitors suppresses growth of experimental tumours more effectively than conventional therapy. The effect of this combination on ovarian cancer remains to be evaluated. Therefore, we investigated the synergism of ginsenoside Rg3 and cyclophosphamide (CTX) on growth and angiogenesis of human ovarian cancer. Methods Twenty-eight female athymic mice were divided randomly into 4 groups of 7: ginsenoside Rg3, CTX, ginsenoside Rg3 and CTX combination and control, after being transplanted with ovarian cancer cells (SKOV-3). The mice were given intraperitoneal injection of ginsenoside Rg3 and CTX for the 10 days following inoculation of SKOV-3 cells. The life quality and number of living days of mice were recorded. The size of tumour, tumour inhibitive rate, life elongation rate, proliferating cell nuclear antigen labelling index (PCNALI), expression of vascular endothelial cell growth factor (VEGF) and microvessel density (MVD) of the tumour tissues were estimated. Results Life quality of mice in ginsenoside Rg3 and combined treatment groups were better and number of living days longer than control. Average tumour weights of each treated group were less than control and there was no significant difference among the treated groups. PCNALI of treated groups was lower than control. The MVD value and VEGF expression in treated groups were significantly lower than control and the MVD values of ginsenoside Rg3 and combined treatment groups were lower than that of CTX group. Conclusions Ginsenoside Rg3 significantly inhibited growth and angiogenesis of ovarian cancer when used alone or combined with CTX. Ginsenoside Rg3 and CTX combination reinforced the antitumour effect each other and improved the living quality and survival time of mice with tumour.  相似文献
2.
血管内皮生长因子最新研究进展   总被引:12,自引:0,他引:12  
张瑞鹏  郭平凡 《医学综述》2008,14(15):2258-2260
血管内皮生长因子(VEGF)是一种能特异的作用于血管内皮细胞的生长因子,它是一种具有促血管生成活性的功能性蛋白。VEGF受体特异性地分布于血管内皮细胞,VEGF通过与其特异性受体的结合,发挥生理功能:①促血管内皮细胞分裂从而促进新生血管形成;②增强血管通透性的功能。其活性的发挥受到多因素、多水平的调节,如缺氧、癌基因、细胞因子、细胞间质成分等。本文从VEGF的促血管形成机制及其调控因素等方面对其生物学行为和特性予以综述。  相似文献
3.
热疗联合放疗对S180细胞凋亡及血管再生的影响   总被引:11,自引:0,他引:11  
目的 探讨热疗联合放疗对小鼠S180肿瘤模型细胞凋亡及血管再生的影响.方法 实验用昆明小鼠60只,右后肢股部皮下接种S180肿瘤细胞株,当肿瘤生长至1cm3时分组进行局部热疗、放疗和热放疗.然后用RTPCR检测Bcl-2 mRNA,免疫组化方法检测调亡细胞,血管内皮生长因子(VEGF)蛋白,以微血管密度(MVD)作为定量检测指标.结果 热疗、放疗、热放疗组细胞凋亡指数较对照组增加(P<0.01),以热放疗组增加最为显著(P<0.01).热疗、放疗、热放疗组Bcl-2基因表达较对照组减弱(P<0.01),以热放疗组减弱最为显著(P<0.01).热疗组VEGF蛋白表达和MVD较对照组降低(P<0.01),放疗组VEGF蛋白表达和MVD较对照组升高(P<0.01),热放疗组VEGF蛋白表达和MVD较放疗组降低(P<0.01).结论 热疗可以下调Bcl-2基因,诱导S180株细胞凋亡,抑制肿瘤细胞VEGF的产生,使MVD下降.与放疗共同作用于肿瘤细胞,可增加肿瘤细胞放射敏感性,对肿瘤有显著的治疗作用.  相似文献
4.
超声微泡介导肝细胞生长因子促进大鼠梗死心肌血管新生   总被引:7,自引:0,他引:7  
目的探讨超声靶向破坏微泡介导肝细胞生长因子(HGF)促进大鼠梗死心肌血管新生的可行性。方法将40只Wistar大鼠制备成心肌梗死模型后随机分为4组:(1)HGF 超声 微泡组(HGF US/MB);(2)HGF 超声组(HGF US);(3)HGF 微泡组(HGF MB);(4)单纯手术组(SA)。于基因转染后14d处死各组大鼠,采用免疫组织化学法(IHC)检测缺血心肌周围CD34表达,并在显微镜下计数心肌内新生微血管密度(MVD)。采用酶联免疫吸附法(ELISA)检测心肌组织内HGF蛋白表达情况,并对心肌内HGF含量与MVD进行相关性分析。结果IHC结果显示,CD34定位于血管内皮细胞胞膜和胞浆,显示为棕黄色或棕褐色颗粒,新生的微血管被染成棕黄色,显微镜下计数每高倍镜视野下的MVD,结果表明在HGF US/MB组心肌中MVD最高,为(266.9±39.8)个/高倍镜视野,与其他各组比较差异均有显著性(P<0.01)。ELISA结果显示HGF在HGF US/MB组心肌中表达最高,为(5.54±0.81)ng/g,且前壁表达高于后壁(P<0.05),与其他各组心肌HGF含量相比差异也均有显著性(P<0.01)。相关分析表明,心肌HGF含量与MVD呈明显正相关。结论超声靶向破坏微泡可介导HGF基因在缺血心肌内的高效转移并促进血管新生,为心肌梗死的基因治疗提供了一个新途径。  相似文献
5.
目的:探讨上皮性卵巢癌中血管内皮生长因子(VEGF)及其受体(flt-1)表达与血管生成和恶性程度的关系.方法:采用免疫组织化学和形态定量及半定量方法检测53例卵巢癌中VEGF和flt-1的表达水平和间质微血管密度(MVD).结果:VEGF及其受体flt-1的表达均与卵巢癌淋巴结转移有密切关系(P<0.05).卵巢癌间质的MVD与淋巴结转移及VEGF表达有关(P<0.01).结论: VEGF及其受体flt-1的表达与卵巢癌淋巴结转移和间质血管生成有密切关系.  相似文献
6.
血管内皮祖细胞研究进展   总被引:6,自引:2,他引:4  
血管内皮祖细胞(EPC)是血管内皮细胞的前体细胞,主要来源于脐静脉血、成人外周血和骨髓,不仅参与胚胎血管形成,而且在出生后的血管生成过程中有很强的促进作用.EPC在血管损伤修复中起重要作用,为缺血性疾病的治疗提供了值得探索的新途径.以下就EPC在缺血心肌、缺血肢体、损伤角膜修复中的血管生成作用作一综述.  相似文献
7.
许扬  赵英凯  毕明刚  刘妍 《中国比较医学杂志》2007,17(12):745-747,F0003
目的应用Image-Pro Plus 5.0图像处理和分析软件,研究鸡胚尿囊膜(chick chorioallantoic membrane,CAM)血管新生面积定量的新方法。方法20只发育良好的7日龄鸡胚,分为龙葵给药组和对照组,每组10只。将中药龙葵水提液及等量蒸馏水吸附于5 mm直径的定性滤纸,置于CAM上。利用Image-Pro Plus 5.0软件,定量血管新生面积、蛋壳开窗处对应的CAM面积,计算出血管新生面积与CAM面积的比值。结果用Image-Pro Plus 5.0可方便、自动、准确地进行给药前后的数据收集和面积计算。统计分析表明,受试物龙葵可明显抑制CAM血管新生,与对照组比较有极显著差异(P<0.001)。结论Image-Pro Plus 5.0图像处理和分析软件是一种高效、准确的统计血管新生面积的工具,用该软件定量蛋壳开窗部位下的血管新生面积占开窗部位所对应的CAM总面积,不仅操作简便,而且数据计算自动生成,可较准确地反映鸡胚血管新生情况。  相似文献
8.
Background Esophageal carcinoma is a common kind of malignant tumor and about 90% of which is esophageal squamous cell carcinoma (ESCC), and it has a high incidence in China. In recent years it has been argued that angiogenesis plays a key role in tumor growth and metastasis and it is a complex process influenced by many factors. This study was aimed to investigate the expression of PC cell-derived growth factor (PCDGF or progranulin) and vascular endothelial growth factor (VEGF) in ESCC tissue and their relationship with clinical pathological parameters of ESCC, clarify the role of PCDGF and VEGF in the angiogenesis of ESCC.
Methods The expression of PCDGF and VEGF in 50 surgical specimens from patients with ESCC and 20 with normal esophageal mucosa were detected by immunohistochemistry. The vascular endothelial cells in tumor tissues were labeled by antibody to CD105 for counting microvessel density (MVD).
Results The expression of PCDGF and VEGF in ESCC was significantly higher than that in normal mucosa. Expression correlated with the depth of tumor invasion, lymph node metastasis, and TNM (classification tumor, nodes, metastasis). In ESCC, both the expression level of PCDGF and VEGF had a positive correlation with MVD and the expression of PCDGF had a significant correlation with the expression of VEGF.
Conclusions These results show that both of PCDGF and VEGE have higher expression in ESCC, which indicate that they have a close relationship with angiogenesis. They may be involved in tumor growth, infiltration and metastasis through promoting tumor angiogenesis and may be an important index reflecting biological behavior and prognosis of ESCC.  相似文献
9.
Inhibitory effect of ginsenoside Rg3 on ovarian cancer metastasis   总被引:5,自引:0,他引:5       下载免费PDF全文
Background Ginsenosides are main components extracted from ginseng, and ginsenoside Rg3 is one of the most important parts. Ginsenoside Rg3 has been found to inhibit several kinds of tumor growth and metastasis. The present study was undertaken to investigate the effect of ginsenoside Rg3 on human ovarian cancer metastasis and the possible mechanism. Methods The experimental lung metastasis models of ovarian cancer SKOV-3 and the assay of tumor-induced angiogenesis were used to observe the inhibitory effects of Rg3 on tumor metastasis and angiogenesis. The effect of Rg3 on invasive ability of SKOV-3 cells in vitro was detected by Boyden chamber, and immunofluorescence staining was used to recognize the expression of matrix metalloproteinase 9 (MMP-9) in SKOV-3 cells. Results In the experimental lung metastasis models of ovarian cancer, the number of tumor colonies in the lung and vessels oriented toward the tumor mass in each ginsenoside Rg3 group, was lower than that of control group. The invasive ability and MMP-9 expression of SKOV-3 cells decreased significantly after treatment with ginsenoside Rg3. Conclusions Ginsenoside Rg3 can significantly inhibit the metastasis of ovarian cancer. The inhibitory effect is partially due to inhibition of tumor-induced an qioqenesis and decrease of invasive ability and MMP-9 expression of SKOV-3 cells.  相似文献
10.
目的研究苏拉明联合顺铂对肺腺癌LA795细胞T739小鼠移植瘤的抑制作用和移植瘤内bFGF表达的影响。方法复制小鼠移植瘤模型,将32只接种高转移性LA795肺腺癌细胞的T739小鼠随机分成4组:对照组、顺铂组、苏拉明组和顺铂+苏拉明组。用药干预16d,用药中观察肿瘤生长情况,于接种后24d处死各组小鼠,取出双肺和剥离皮下肿瘤,计算出肺转移发生率,计数各组小鼠肺表面转移结节数及算出肺表面结节转移抑制率。移植瘤标本行病理观察,免疫组化和图像分析系统定量检测肿瘤组织微血管密度(MVD)及碱性成纤维细胞生长因子(bFGF)表达。结果各用药组肿瘤的生长受到抑制,瘤重明显低于对照组,其抑瘤率分别为23.03%、34.40%和56.30%。苏拉明组与对照组比肺表面转移结节数、肺转移发生率下降,肺表面结节转移抑制率上升,联合组更为明显。病理观察见各用药组肿瘤细胞出现坏死、苏拉明组及联合组肿瘤间质中血管数减少。苏拉明组,顺铂+苏拉明组MVD、bFGF的表达都比对照组减少,差异有显著性(P〈0.01);两者联合有协同下调MVD、bFGF表达的作用,而单用顺铂组与对照组比差异无显著性。结论苏拉明可明显抑制肺腺癌细胞在小鼠体内的生长和转移,与顺铂有协同作用,其机制可能与下调bFGF表达,抑制其微血管形成有关。  相似文献
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