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81.
AIM:To investigate therapeutic effects of recombinant human growth hormone(rhGH) on rat sepsis and its possible mechanisms.METHODS:Mean arterial pressure (MAP), levels of plasma TNFα, IL-1β and endotoxin, leukocyte count and survival rate within 1 week were determined after E. coli injection among control group, sepsis group and sepsis+rhGH group.RESULTS:(1)rhGH diminished the decrease of MAP, reduced plasma endotoxin and TNFα levels and increased neutrophil ratio in total leukocytes in sepsis rat. rhGH increased survival rate within 1 week on sepsis rat. (2)No changes were found in IL-1β level among the three groups.CONCLUSION:rhGH showed desirable beneficial effects on rat sepsis, which may attribute to: improving circulatory function;maintaining intestinal mucosa barrier, attenuating bacteria/endotoxin translocation and inhibiting the production and release of TNFα.  相似文献   
82.
83.
渭河阶地全新世土壤粒度成分高分辨率研究   总被引:2,自引:7,他引:2  
通过对渭河阶地全新世土壤的野外考察和粒度成分的高分辨率分析研究,揭示了该区域褐色土的成壤作用过程与季风气候变化的关系。研究表明渭河第二级阶地褐色土形成在全新世气候最适宜期(8500-3100a B.P.),从8500a B.P.开始该土壤开始发育,老官台文化兴起。从3100a B.P.开始的气候干旱化和沙尘暴堆积形成了黄土L。层。西周时期对应于该干旱期的初期。  相似文献   
84.
稻象甲的防治指标和防治适期研究   总被引:2,自引:1,他引:2  
根据稻象甲虫量与水稻产量的关系 ,结合现行的稻谷价格 ,产量水平和防治费用等因素 ,进行了稻象甲危害损失的测定 ,制定了稻象甲的防治指标。采用累积虫日作为防治指数 ,确定了在江西境内稻象甲的防治适期  相似文献   
85.
苏云金芽孢杆菌cry基因在大肠杆菌中表达产物和生物活性   总被引:4,自引:0,他引:4  
研究了几种Bt cry基因于大肠杆菌(Escherichia coli)中表达产物在pH 10.0的50mmol/L碳酸钠和20mmol/L乙醇胺溶解液中的溶解性 ,发现同样的Cry蛋白在碳酸钠中的溶解度大于乙醇胺。通过胰蛋白酶消化 ,明确Cry1Ca7、Cry1Ia8酶解产物为 38kD多肽 ;Cry1Ie1、Cry1Cb2、Cry2Ab4酶解产物为 41kD多肽 ;Cry1Ac酶解产物为60kD多肽。采用FPLC层析方法对 6种原毒素及其酶解后得到的毒素多肽进行了分离纯化 ,比较了原毒素和毒素的杀虫活性的差异。其结果表明 ,Cry1Ac的原毒素和毒素对棉铃虫初孵幼虫的校正死亡率均为 100% ,Cry2Ab4的原毒素的毒力高于其酶解毒素。  相似文献   
86.
综述了非放射性地高辛(DIG)标记系统的原理和主要特点,介绍了地高辛标记核酸探针的主要标记方法,影响探针标记方法选择的因素,标记探针的显色检测方法及其在食用菌研究领域的应用。  相似文献   
87.
AIM:To investigate the effect of the heat shock response on the reperfusion arrhythmias(RAs) and the possible mechanism involved. METHODS:Fifty-five Sprague Dawley rats were randomly divided into 2 groups: the heat shock group (group H,n=29) and the control group (group C,n=26). The rats in group H were preconditioned with heat shock 24 hours before, and that in group C were not. The hearts of 16 rats in group H and 16 in group C were exercised and mounted on a non-circulating Langendorff perfusion apparatus and perfused retrogradely with modified K-H buffer and mimic ischemia/reperfusion was applied. Additionally, conventional intracellular microelectrode techniques were used for recording such electrophysiological parameters as resting potential(RP), action potential amplitude(APA), over shot(OS), maximum depolarization velocity(Vmax) of the hearts of other 13 rats in group H and 10 in group C. RESULTS:①Prior heat stress significantly decreased reperfusion arrhythmia. ②The amount of CK release in the effluent in group H was much less than that in group C. ③Myocardial HSP70 content was elevated significantly in group H. ④Heat stress significantly increased myocardial anti-oxydases activity and decreased lipid peroxydative products. Additionally, heat stress significantly reduced the Vmax of action potential. It indicated that rapid Na+ channel of papillary muscles may be inhibited by heat shock. The degree of change of Vmax after ischemia in H group was significantly less than that in group C. And the time of reperfusoin with Tyrode's solution till the action potential appeared as large as that before perfusion with mimic ischemic solution is shorter in group H than in group C. CONCLUSION:Heat shock pretreatment markedly reduces ischemia/reperfusion-induced injury of heart and ventricular arrhythmias in rats and this effect may be associated with the inhibition of rapid Na+ channel of papillary muscles by heat shock and the increase in myocardial HSP70 and anti-oxydase activity.  相似文献   
88.
AIM:To investigate the effect of lansoprazole on gastric ulceration in rats. METHODS:Using the gastric ulcer model induced by hemorrhagic shock, restraint water-immersion stress and pylorus-ligature, the protective effect of lansoprazole (iv) on gastric ulceration was observed. RESULTS:Pretreatment with lansoprazole (7.5-60 mg/kg) significantly inhibited the formation of gastric ulcer in the three models in a dose-dependent manner. The autiulcer efficacy of lansoprazole was similar to that of omeprazole in the equal dose, but stronger than that of omeprazole for ulcer induced by water-immersion stress.CONCLUSION:The intravenously administered lansoprazole inhibited formation of experimental gastric ulcer in rats.  相似文献   
89.
AIM:To investigate the effect of Se-containing spirulina phycocyanin (Se-SPC) on liver injury of mice induced by carbon tetrachloride (CCl4). METHODS:The mouse model was conducted by intragastric feeding with 2% CCl4 oil for three times, meanwhile Se-SPC, spirulina phycocyanin (SPC) and Na2SeO3 were injected (ip) to various groups for 7 days. Then selenium (Se), glutathione peroxidase (GPx), superoxide dismutase (SOD), alanine aminotransferase (ALT), malondiaoldehyde (MDA) and nitric oxide (NO) levels in blood and liver were measured. RESULTS:The level of Se,GPx and SOD activities were obviously higher(P<0.05)but ALT activity,MDA and NO2-/NO3- levels were remarkably lower(P<0.05)in Se-SPC treated groups than those in CCl4 groups,and effects of high dose Se-SPC on Se,GPx,MDA and NO2-/NO3- were even more significant(P<0.01).Under the same dose of Se or protein,effects of all selected targets in Se-SPC groups were more efficient than those in SPC groups and inorganic-Se groups.Furthermore,Se levels had a positive correlation with GPx activity(r=01705),which had negative correlation with levels of MDA,NO2-/NO3- and ALT(r=-0.629,r=-0.336,r=-0.457,respectively), and positive correlations between ALT activity and MDA or NO2-/NO3- level were found (r=0.519,r=0.641). CONCLUSION:These results indicated that Se-SPC may attenuate liver injury of mice induced by CCl4 through its anti-inflammatory action and enhancing selenoenzyme expression.  相似文献   
90.
Protein kinase C pathway is an important intracellular signal transduction pathway. A growing number of evidences showes that activation of PKC influences endothelial cell permeability. In this review, we briefly summarize the effects and regulating pathways of protein kinase C in modulation of vascular endothelium permeability.  相似文献   
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