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921.
人工同龄纯林树冠面积比例系数计算及林分标准密度(立木株数)确定的研究 总被引:4,自引:0,他引:4
人工同龄纯林树冠面积比例系数计算及林分标准密度(立木株数)确定的研究熊奎山(甘肃省林业勘察设计研究院兰州730020)关键词人工同龄纯林,树冠面积比例系数,林分标准密度确定Reineke(1983)指出:具有完满立木度的同龄纯林,具有相同的单位面积株... 相似文献
922.
兔颈动脉窦和颈动脉体的神经支配 总被引:1,自引:1,他引:0
用HRP法对兔颈动脉窦和颈动脉体的神经支配进行了分析,表明,支配颈动脉窦和颈动脉体的标记细胞均出现于舌咽神经远节和颈上节。颈动脉体感觉传入中枢突终未见于延髓闩部邻近极后区的腹外侧,颈上节的标记细胞分布于尾侧半部。提示颈动脉窦和颈动脉体对心血在管活动的调节存在着经舌咽神经将感觉传入中枢的通路和经颈上节进行交感神经活动支配的传出通路。为研究心和管生理提供了形态学资料。 相似文献
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AIM: To evaluate the alterations in calcium metabolism of the vascular smooth muscle in the late phase of septic shock and test the hypothesis that nitric oxide might be involved in sepsis-induced vascular hyporeactivity. METHODS: Male Sprague-Dawley rats were subjected to sepsis by cecal ligation and puncture (CLP). 18 hours post CLP, rat aortic rings were employed for measurement of contractile responses by using organ bath technique. RESULTS: In endothelium-denuded aortic rings from CLP rats, concentration-contraction curves to phenylephrine (PE) and KCl were significantly decreased when compared to that from sham control rats. The transient contraction induced by PE in calcium-free Krebs solution and the concentration-dependent contraction to CaCl2 in KCl-depolarized medium were also markedly reduced. The hyporeactivity was partially reversed by treatment with aminoguanidine, a selective inducible nitric oxide synthase inhibitor. CONCLUSION: An impairment in calcium handling in vascular smooth muscle is involved in the vascular hyporeactivity during the late phase of septic shock, in which an excessive nitric oxide production might be the major mechanism. 相似文献
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Li M Liang CG Xiong B Xu BZ Lin SL Hou Y Chen DY Schatten H Sun QY 《Domestic animal endocrinology》2008,34(4):360-371
Previous studies have shown that epidermal growth factor (EGF) has the ability to promote in vitro cultured porcine oocyte maturation. However, little is known about the detailed downstream events in EGF-induced meiotic resumption. We designed this study to determine the relationship of EGF, EGFR, phosphatidylinositol 3-kinase (PI3-kinase), MAPK, and germinal vesicle breakdown (GVBD) during oocyte maturation. Our results showed that GVBD in cumulus-enclosed oocytes (CEOs) but not in denuded oocytes (DOs) was induced by EGF in a dose-dependent manner, which indicated that cumulus cells but not oocyte itself were the main target for EGF-induced meiotic resumption. Furthermore, we found that MAPK in cumulus cells rather than in oocyte was activated immediately after EGF administration. To explore whether EGF exerts its functions through MAPK pathway, the activities of EGF receptor (EGFR) and MAPK were inhibited by employing AG1478 and U0126, respectively. Inhibition of MAPK blocked EGF-induced GVBD, whereas inhibition of EGFR prevented MAPK activation. Both AG1478 and U0126 could lead to the failure of EGF-induced GVBD singly. Notably, we found that LY294002, a specific inhibitor of PI3-kinase, effectively inhibited EGF-induced MAPK activation as well as subsequent oocyte meiotic resumption and this inhibition could not be reversed by adding additional EGF. Thus, PI3-kinase-induced MAPK activation in cumulus cells mediated EGF-induced meiotic resumption in porcine CEOs. Together, this study provides evidences demonstrating a linear relationship of EGF/EGFR, PI3-kinase, MAPK and GVBD and presents a relatively definitive mechanism of EGF-induced meiotic resumption of porcine oocyte. 相似文献
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Mast cell mediated inflammatory response in chickens after infection with very virulent infectious bursal disease virus 总被引:1,自引:1,他引:0
Wang D Xiong J She R Liu L Zhang Y Luo D Li W Hu Y Wang Y Zhang Q Sun Q 《Veterinary immunology and immunopathology》2008,124(1-2):19-28
The potential role of the mast cells in the invasion of very virulent infectious bursal disease virus (vvIBDV) is unknown. We evaluated mast cell activity and tryptase production after vvIBDV infection in special pathogen-free (SPF) chickens using cytochemistry and immunohistochemistry analyses. The results were as follows: (1) severe histologic lesions were observed in the thymus, spleen, cloacal bursa, liver, kidney and other tissues. vvIBDV viral antigens were detected and presented extensively in the parenchymatous organs, in particular, the cloacal bursa, liver, kidney, thymus, spleen and pancreas. (2) In the vvIBDV-infected group, the mast cell population increased markedly in the liver, kidney, thymus, glandular stomach, spleen and cloacal bursa on days 1, 2 and 3 after vvIBDV infection (p<0.05). However, very few mast cells were observed in those same tissues in the controls, especially in the bursa of Fabricius. (3) Tryptase, a marker for activated mast cells, has a positive correlation with mast cell distribution. The mast cells identified in the tissues were likely to be activated since they were associated with cell degranulation and the presence of tryptase. Furthermore, the co-localization of mast cells, and presence of vvIBDV antigens suggests that the mast cells were activated by vvIBDV infection. Our results also suggest that tryptase may contribute to the inflammation of acute IBD induced by vvIBDV infection. Our research contributes to the further understanding of inflammatory response mechanisms and the contribution of mast cell activity to this process. 相似文献
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