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51.
主要探讨中药制剂四生散对人肺癌A5 4 9细胞株的增殖抑制作用以及其急性毒性.应用改进的MTT法测定四生散对肺癌细胞增殖的影响;采用琼脂糖凝胶电泳测定四生散对诱导肿瘤细胞凋亡的影响;再用分剂量组灌胃小鼠的方法,鉴定四生散的急性毒性.实验结果表明,四生散对人肺癌A5 4 9细胞株的增殖有较强的抑制作用,并具有明显的量效和时效相关性;经四生散处理后的A5 4 9细胞呈现凋亡特征性电泳条带;在3 2倍于人的剂量时,小鼠饮食和体重均在正常水平,并无异常,证实口服四生散无急性毒性. 相似文献
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应用免疫组化和突变分析方法,分析晚期胃癌原发灶和转移灶nm23,S100A4和p53的表达差异,探讨肿瘤内部异质性在胃癌转移发生中的意义。结果发现转移抑制基因nm23在转移灶中的表达显著上调,转移促进基因S100A4在转移灶中的表达显著下调,癌基因p53在两者中的表达和突变没有明显差异。nm23在原发瘤中的表达下调以及S100A4和p53的过度表达与胃癌的高侵袭性显著相关。数据显示:nm23和S100A4在胃癌的转移中发挥作用,而p53是胃癌发生的一个晚期事件。 相似文献
54.
转录靶向性KDR启动子调控双自杀基因治疗肺癌的实验研究 总被引:2,自引:0,他引:2
从人肺癌细胞株中克隆KDR基因的启动子(kinasedomainreceptorpromotor,KDRp),构建KDR基因启动子调控的双自杀基因(CDglyTK)真核表达质粒pcDNA3-KDRp-CdglyTK,将其导入ECV304、L9981和NL9980细胞,建立相应的转基因细胞系,并应用不同的前药处理。体内、外实验结果显示:KDR启动子调控的双自杀基因在KDR高表达人肺癌细胞和人脐静脉内皮细胞靶向表达,而在KDR不表达的正常细胞或正常血管内皮细胞中未检测到双自杀基因表达;联合应用5-FC和GCV处理,对转双自杀基因细胞的杀伤作用显著高于单独应用5-FC或GCV,且二者显示了良好的药物协同作用。 相似文献
55.
兰倩 《佛山科学技术学院学报(自然科学版)》2007,25(5):71-74
对牙周非手术基础治疗后进入维护治疗期的22名慢性牙周炎患者进行9个月的纵向观察。每3个月给予口腔卫生宣教,龈上下洁刮治和根面平整,并在基线和每次复查时记录临床检查指标。结果表明:活动性位点的年发生率为5.75%,上下颌磨牙及上颌前磨牙为活动性破坏好发牙位。附着增加的位点数和增加的量随基线袋深增加呈增多趋势,X-Ray检查牙槽骨高度无明显变化,活动性位点螺旋体数量明显多于非活动性位点。说明非手术基础治疗配合定期维护,在较短观察期内可使大多数位点临床指标保持稳定甚至好转,但不能带来明显的骨量增加。 相似文献
56.
A variety of viral-based and immune cell therapies have been proposed for use in the treatment of cancer. One possible approach
to improve the effectiveness of these biological agents may be to combine them such that we can take advantage of natural
immune cell-pathogen relationships. Here we discuss these potential approaches with particular emphasis on the use of immune
cells as carrier vehicles to deliver viral therapies to the tumor.
Received 15 December 2006; received after revision 28 January 2007; accepted 5 March 2007 相似文献
57.
Lanigan F O'Connor D Martin F Gallagher WM 《Cellular and molecular life sciences : CMLS》2007,64(24):3159-3184
During its lifetime, the mammary gland undergoes many phases of development and differentiation. Much of this occurs during
puberty, when the ductal epithelium expands by branching morphogenesis, invading the surrounding fat pad to form an organised
mammary tree. Throughout its existence, the epithelium will go through several cycles of proliferation and cell death during
pregnancy, lactation and involution. Many of the signalling mechanisms which control the initial invasion of the fat pad by
the epithelium, and regulate its continuing plasticity, can be harnessed or corrupted by tumour cells in order to support
their aberrant growth and progression towards invasion. This is true not just for the epithelial cells themselves but also
for cells in the surrounding microenvironment, including fibroblasts, macrophages and adipocytes. This review examines the
complex web of signalling and adhesion interactions controlling branching morphogenesis, and how their alteration can promote
malignancy. Current in vivo and in vitro mammary gland models are also discussed. (Part of a Multi-author Review) 相似文献
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Crnković-Mertens I Wagener N Semzow J Gröne EF Haferkamp A Hohenfellner M Butz K Hoppe-Seyler F 《Cellular and molecular life sciences : CMLS》2007,64(9):1137-1144
Cancer cells are typically characterized by apoptosis deficiency. In order to investigate a possible role for the anti-apoptotic
livin gene in renal cell cancer (RCC), we analyzed its expression in tumor tissue samples and in RCC-derived cell lines. In addition,
we studied the contribution of livin to the apoptotic resistance of RCC cells by RNA interference (RNAi). Livin gene expression was detected in a significant portion of RCC tumor tissue specimens (13/14, 92.9%) and tumor-derived cell
lines (12/15, 80.0%). Moreover, targeted inhibition of livin by RNAi markedly sensitized RCC cells towards proapoptotic stimuli, such as UV irradiation or the chemotherapeutic drugs
etoposide, 5-fluorouracil, and vinblastine. These effects were specific for livin expressing tumor cells. We conclude that livin can contribute significantly to the apoptosis resistance of RCC cells. Targeted inhibition of livin could represent a novel therapeutic strategy to increase the sensitivity of renal cancers towards pro-apoptotic agents.
Received 30 November 2006; received after revision 22 February 2007; accepted 20 March 2007 相似文献
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