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21.
Wistar大鼠160只,随机分为8组,正常对照组、6h组、12h组、24 h组、3d组、5d组、7d组、14d组,每组各20只,除对照组外其他各组大鼠均手术使其一侧后肢股骨粉碎性骨折,各时段组大鼠采血测凝血指标:凝血酶原时间(PT)、凝血活酶时间(TT)、纤维蛋白原(FBG)后取患肢血管做病理学检查.两项检查结果表明,大鼠粉碎性骨折后,12 h至3d内的时间段是肢体深静脉血栓(DVT)形成的关键期,此后进入静脉血栓脱落导致肺栓塞的危险期,在骨折前或骨折后的前3d采取积极措施预防DVT可取得较理想的效果.动态监测创伤骨折大鼠凝血指标的变化,对早期预防创伤后深静脉血栓形成具有诊断价值. 相似文献
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为了研究阶段水分亏缺(亏水+不亏水WLWH、不亏水+亏水WHWL、亏水+亏水WLWL、不亏水+不亏水WHWH)和不同施氮量(NZ:0,NL:0.2 g/kg,NH:0.4 g/kg)对小桐子生长、生理指标和灌溉水利用效率的影响,通过盆栽试验,发现WLWH的生长和灌溉水利用效率均显著高于WHWL;作物的灌溉水利用效率随施氮量的增大而呈现先增大后减小的趋势,在NL水平下达到最大值;与高水高氮的处理NHWHWH相比,中水低氮处理NLWLWH节约灌溉水27%,节约氮肥使用量50%,小桐子株高减少31%、总干物质量减少35%,灌溉水利用效率减少13%,但茎粗增加13%,根冠比增加20%.可见小桐子在第一阶段处理(40~90 d)幼树期对水分的需求量较小,适度的亏缺灌溉可提高灌溉水利用效率;小桐子在第二阶段处理(90~140 d)处于旺长期,对水分的需求量较大,增大灌水量可大幅度促进小桐子生长及其干物质量的积累.全生育期实施亏缺灌溉,可提高小桐子自身适应外界环境能力,抗干旱胁迫能力也逐渐增强,但WLWL水平下的小桐子生长缓慢.经综合分析,认为处理NLWLWH可作为干旱地区条件下的小桐子灌溉和施氮制度. 相似文献
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AIM: To observe the mechanisms of RhoA on vascular reactivity following hemorrhagic shock (HS) in rats. METHODS: The superior mesenteric artery (SMA) in rats subjected to hemorrhagic shock was adopted to assay the vascular reactivity via observing the contraction initiated by norepinephrine (NE) with isolated organ perfusion system. Meanwhile, the effects of Rho kinase, myosin light chain phosphatase (MLCP), myosin light chain kinase (MLCK) on RhoA regulating vascular reactivity were observed. The effects of RhoA agonist U-46619 and inhibitor C3 enzyme on the activities of Rho kianse, MLCP, MLCK and phosphorylation of MLC20 in the vascular smooth muscle cells (VSMC) with hypoxia were also measured. RESULTS: As compared to control group, the cumulative dose-response curves of SMA to NE at 2 h after shock shifted to the right, the maximal contractions (Emax) of NE was significantly decreased. RhoA agonist U-46619 increased the vascular reactivity in the late period of shock. C3 enzyme abolished U-46619 induced the increase in the contractile response of SMA to NE. Rho kinase inhibitor Y-27632 decreased U-46619-induced the increase in the vascular reactivity, MLCP inhibitor calyculin further promoted the increase in the vascular reactivity. However, MLCK inhibitor had no effect on the U-46619-induced change of vascular reactivity. After hypoxia, the activities of Rho kinase and MLCK, and the level of MLC20 phosphorylation were decreased, MLCP activity was increased. RhoA agonist U-46619 increased the activity of Rho kinase and phosphorylation of MLC20, decreased the activity of MLCP, but had no effects on MLCK activity. CONCLUSION: RhoA plays an important role in the regulation of vascular reactivity following shock. The mechanism is closely related to regulating the activities of Rho kinase and MLCP, and increasing the phosphorylation of MLC20 in VSMC. 相似文献
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为深入了解桉树生态水文过程,正确认识桉树水文功能,本文通过野外实测法,对不同林龄尾巨桉林下穿透雨进行连续观测,并结合林外降雨量分析尾巨桉人工林林下穿透雨特征及其与降雨的关系.结果发现:尾巨桉各林龄林下穿透雨量与降雨量呈极显著正相关线性模型(P<0.01);林下穿透雨率与降雨强度呈极显著正相关(P<0.01),截留率与降雨强度呈极显著负相关(P<0.01),变异系数随降雨强度的增大先增大后减小,且两者均与降雨量无显著相关性;干湿季林下穿透雨率差异显著,湿季显著大于干季(P<0.05),最大穿透雨率及最小穿透雨率分别是干季的1.17倍和3.2倍. 相似文献
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XI Yu-hui MENG Qing-wei XU Chang-qing WANG Li-na LIN Yan LI Hong-zhu ZHANG Li 《园艺学报》2010,26(5):844-847
AIM: To investigate the expression and function of sirtuin 1 (Sirt1), one of the class III histone deacetylases, in hypertrophied mouse myocardium induced by isorenin (ISO). METHODS: The Kunming mice were randomly divided into 3 groups: control group, ISO group and ISO+nicotinamide (NAM) group. The myocardial hypertrophy was induced by dorsal subcutaneous injection of isorenin. Nicotinamide, an inhibitor against Sirt1, was given by peritoneal injection. Heart weight index (heart weight/body weight), hematoxylin and eosin staining, transmission electron microscope and mRNA expression of brain natriuretic peptide (BNP) were observed to identify the myocardial hypertrophy. The expression of Sirt1 in mRNA and protein levels was detected by RT-PCR and Western blotting, respectively. RESULTS: Compared to control group, the results of heart weight index, hematoxylin and eosin staining, the observation of transmission electron microscopy and mRNA expression of BNP showed that the mouse myocardial hypertrophy was induced by isorenin successfully. The Sirt1 expression was increased in hypertrophy model group (P<0.01 vs control group). Treatment with nicotinamide inhibited the cardiac hypertrophy induced by ISO (P<0.05 vs ISO group) and decreased the expression of Sirt1 (P<0.01 vs ISO group). CONCLUSION: Activation of Sirt1 might be involved in the process of myocardial hypertrophy stimulated by isorenin in mice. 相似文献
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