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11.
魏俊峰 《上海交通大学学报(农业科学版)》2015,(5):47-50
拟在动态平衡的视角下对现代足球阵型的演变历程进行梳理与整合,希望对阵型之间的关联及其对足球运动发展的影响提供见解,对阵型演变的不同阶段进行探讨,探寻足球攻守平衡与不同阵型的嬗变关系,同时也为推动未来足球阵型演变对战术打法的影响研究提供参考依据。采用文献资料、系统分析、专家访谈和逻辑分析等方法,对现有的足球阵型发展的概况进行分析之后,认为现代足球阵型的演变历程不断交替出现攻守的平衡与不平衡,正是交替出现的状况促进了阵型的改变,进而影响了阵型的发展。当阵型的发展过程中出现攻守平衡时,就有其它后来者对该阵型进行学习、模仿、改进、提高。当阵型的发展过程中出现攻守不平衡,攻强于守或者守强于攻时,就会促进阵型的演变向攻守平衡的方向发展,因此就会出现阵型的发展处于不平衡-平衡-不平衡-再到平衡的态势,从而形成比赛阵型发展本身的稳定与不稳定状态交替出现。研究认为,世界足球阵型演变的过程是一种动态的、不断发展的、维持某种平衡与稳定的、平衡和不平衡交替运动的情况,即动态平衡的状态。提出将现代足球阵型演变的过程分为不同的阶段,每一个阶段内,都分别出现攻守平衡与攻守不平衡的状态,而这种平衡与不平衡的存在与区别、斗争与转化正是足球阵型演变与发展的规律。 相似文献
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AIM: To investigate the effects of chronic hypoxia on the aggressiveness of MCF-7, a human breast cancer cell line, and the underlying mechanisms.METHODS: MCF-7 cells were cultured under hypoxia (1% O2, 5% CO2 and 94% N2) or control (95% O2 and 5% CO2) condition. The viability, proliferation, and invasion and migration abilities of the MCF-7 cells were determined by MTT assay, CCK-8 assay, cell counting, and cell invasion and migration assays. Anchorage-independent growth and the alteration of cellular polarization of the MCF-7 cells were tested by soft agar colony formation assay and Matrigel-3D culture assay, respectively. The effects of chronic hypoxia on the growth and metastasis of MCF-7 cells in vivo were investigated by xenograft in nude mice. The morphological changes of the MCF-7 cells were observed under an inverted microscope. Hypoxia-induced alterations in the levels of hypoxia inducible factor-1 (HIF-1) and phosphorylated glycogen synthase kinase-3β (p-GSK-3β) as well as epithelial-mesenchymal transition (EMT) molecules, such as E-cadherin, N-cadherin, vimentin, matrix metalloproteinase (MMP)-3 and MMP-9, were determined by Western blot.RESULTS: Chronic hypoxia significantly increased the viability, proliferation, and invasion and migration abilities of MCF-7 cells in vitro, enhanced the anchorage-independent growth, facilitated cellular polarization alteration in Matrigel-3D culture, and promoted cancer metastasis in vivo. Hypoxia up-regulated HIF-1, activated GSK-3β, down-regulated E-cadherin and increased the protein levels of N-cadherin, vimentin, MMP-3 and MMP-9. CONCLUSION: Chronic hypoxia enhances the aggressiveness of breast cancer cells probably through EMT. 相似文献
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AIM: To observe the influence of gold nanoparticles combined with Endostar (AuNPs-Endostar) on the melanoma lung metastasis of mice and the underlying mechanism. METHODS: C57BL/6 mice (n=24) were selected for constructing the model of spontaneous lung metastasis of melanoma B16-F10 cells. Subsequently, the mice were randomly divided into Endostar group, AuNPs group, AuNPs-Endostar group and model group. After the formation of melanoma, the mice in each group were injected with different drugs through tail vein for 0.1 mL daily. After 9 d, the mice were narcotized for cutting the tumors in situ. After the operation, they were raised for 2 weeks before killed for obtaining the lung tissues to observe the situation of the metastasis. HE staining was utilized for observing the necrosis status of the tumors in situ, while immunostaining was applied for testing the expression of CD31, carbonic anhydrase-IX (CA-IX), vimentin and zonula occludens-1 (ZO-1) in the tumors. RESULTS: Compared with model group, the pulmonary metastasis in the groups with medical treatment was obviously reduced. In AuNPs-Endostar group, the metastasis inhibition rate was the highest, and the tumor necrosis was also decreased obviously, with the significant reduction of CD31, CA-IX and vimentin expression in the tumors and significant increase in ZO-1 expression. CONCLUSION: Compared with using Endostar or AuNPs alone, the combination of AuNPs with Endostar significantly improves the curative effect of inhibiting the pulmonary metastasis of melanoma in the mice. The mechanism may be related to reducing the tumor angiogenesis, norma-lizing the blood vessels and improving tumor hypoxia, thus inhibiting the tumor epithelial-mesenchymal transition, increasing the tight junctions between tumor cells and decreasing the invasiveness. 相似文献
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Thavat M 《Asia Pacific viewpoint》2011,52(3):285-298
Fair-trade and organic products are often sold at price premiums justified by smaller production volumes that are associated with greater social and environmental responsibility. The consumption of these products confers on the consumer a greater sense of morality – and usually a claim to better taste. This paper tells the story of attempts to promote organic/fair-trade rice production by de facto organic Cambodian farmers for export to North American and European markets in order to assist poor farmers to trade their way out of poverty. It demonstrates that instead of promoting sustainable agriculture and fair trade between developed and developing markets, organic/fair-trade projects may impose First World consumer ideals and tastes that are out of step with the larger realities of agrarian transition in Cambodia and the wider region of developing Southeast Asia. 相似文献
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AIM: To investigate the role of voltage-dependent anion channel (VDAC) in H9c2 cardiomyocytes subjected to anoxia/reoxygenation (A/R).METHODS: The shRNAs targeting VDAC1 mRNA were inserted into pSUPER plasmid.H9c2 cells were randomly divided into 5 groups as follows: control group, A/R group, anoxia preconditioning (APC) group, pSUPER-VDAC1-A/R group and pSUPER-A/R group. The expression of VDAC1 was detected by Western blotting. Cellular injury was evaluated by measuring the cell viability and the release of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK). The mitochondria membrane potential was determined by flow cytometry.RESULTS: VDAC1 expression was up-regulated in A/R group and was inhibited in APC group. Similarly, down-regulation of VDAC1 expression by shRNA protected H9c2 cells from A/R injury. Moreover, we found that, with silencing VDAC1 expression, mitochondrial membrane potential was well preserved in H9c2 cells subjected to A/R.CONCLUSION: Down-regulation of VDAC1 protects H9c2 cells against A/R injury and its possible mechanism appears to be related to the regulation of mitochondial permeability transition pore opening. 相似文献
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