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61.
AIM:To establish rat chronic obstructive pulmonary disease(COPD) models by passive cigarette smoking plus intratracheal instillation of lipopolysacchride(LPS) or passive cigarette smoking only, which would be similar to the pathogenesis of human COPD. METHODS:48 Wistar rats were randomly divided into 4 groups.(1) Healthy control I group(n=12), rats were bred 4 weeks;healthy control II group(n=12), rats were bred for 3months. (2) Model group I (n=12), 200μg lipopolysaccharide(LPS) was instilled intratracheally once for every two weeks and the rats were exposured to 5% of cigarette smoke, 0.5 h/d for 4 weeks.(3) Model group II(n=12),rats were exposed to 5% of cigarette smoke, 0.5 h/d for 3 months. The pathologic changes of airways and lung tissues, pulmonary function and blood gas analysis were determined. The airway wall lymphocytes and alveolar macrophages were counted. The cross areas of epithelial layer, smooth muscle layer and lamina propria of bronchi were measured. The hydroxyproline of lung tissue homogenates was determined by biochemistry method.RESULTS:The pathologic changes of airways and lung tissue of two models were similar to but milder than those of COPD patients(biopsy data). The collagen deposition and the cross areas of epithelial layer and smooth muscle layer in airway walls of two model groups were significantly increased than those of control groups(P<0.01,P<0.05).FEV0.3/FVC% of two model groups, PaO2 and SaO2 of model I group were significantly decreased, while Ri and Re in model I group were significantly increased than that of control I group(P<0.05). The PaCO2 and the counts of lymphocytes and alveolar macrophages of both model groups were significantly increased than those of the control groups (P<0.01). Lots of alveolar macrophages had phagocyted smoke granules. The amounts of hydroxyproline of two model groups were significantly increased than those of control group((P<0.05) and were negatively related to the FEV0.3/FVC%, respectively (P<0.01,P<0.01) and positively related to airway resistance of model I group(P<0.01). CONCLUSIONS:COPD rat models were successfully established by passive cigarette smoking plus intratracheal instillation of LPS and cigarette smoking only. The pathologic changes were similar but milder than those of COPD patients. The airway obstruction of model I group was more severe than that of model II group, but they have no significant difference. 相似文献
62.
AIM: To study the electrophysiological characteristics of ion channels of stem cell derived cardiomyocytes(SCDC) of mouse. METHODS: Embryonic stem cells of D3 line(ES-D3) were cultured on the MEF feeder layer with BRL conditioned medium, and fetal mouse heart cells(FMHC)were cultured in vitro. Then ES-D3 cells were induced to differentiate into many kinds of cells. SCDC were harvested on day 12 after differentiation initiating and identified by electro-microscope and immunocytochemistry. SCDC and FMHC were prepared for the patch-clamp research. Sodium and calcium currents together were elicited and compared between SCDC and FMHC. RESULTS: The current characteristics of sodium and calcium channels of SCDC were very similar to FMHC. CONCLUSION: The functional expression of ion channels occurred during ES-D3 cells differentiation and the electrophysiological characteristics of sodium and calcium channels of SCDC are very similar to FMHC. 相似文献
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采用均匀设计法优化红汁乳菇液体深层发酵培养基。结果表明,最佳培养基配方是:蔗糖34g]L,废糖蜜13mL/L,麸皮36g/L,玉米粗粉20g/L,KH2PO43g/L,菌丝体最大生物量达18.087g/L。 相似文献
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武夷菌素对番茄灰霉菌的抑制作用及对番茄抗病性相关酶活性的影响 总被引:3,自引:0,他引:3
采用凹陷载玻片法测定了武夷菌素对番茄灰霉菌分生孢子萌发的抑制作用,在离体番茄叶片上测定了被武夷菌素处理后的番茄灰霉菌菌丝和分生孢子致病性的变化以及武夷菌素对番茄幼苗体内抗病性相关酶活性的影响。结果表明:武夷菌素对番茄灰霉菌的分生孢子有较强的抑制作用,其EC50为14.1μg/mL。浓度为100μg/mL的武夷菌素可完全抑制孢子的萌发。武夷菌素能使灰霉菌菌丝和分生孢子的致病性明显下降,同时还能诱导番茄体内抗病性相关酶(SOD、POD、PPO、PAL)活性的增强,提高番茄幼苗的抗病性。 相似文献
68.
AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (105 U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC. 相似文献
69.
中国北方沙尘天气原因探讨 总被引:2,自引:1,他引:2
我国是沙尘暴易发的国家,进入20世纪90年代以来,强沙尘暴有频率增加、强度加大、范围扩展、危害程度加剧的趋势。沙尘暴的发生危害范围亦逐渐从西北干旱经济落后区扩展到经济发达的北京、天津及华北平原区,近年来的沙尘暴造成了社会经济和人民生命财产的重大损失。受大气环流场和季风气候类型影响,中国冬、春盛吹西北风,强劲而干燥。发生沙尘暴的天数与大风日数和地面热力稳定程度相关,3-5月中国西北内陆地表增温大,是风力场和热力场极不稳定的季节,地表气候容易发生蠕动,沙尘暴便由此启动并易发。除自然要素外,不合理的人类活动也将诱发沙尘暴天气的发生,有些情况下还起到比自然要素更重要的作用。从生态地理区域的角度看,沙尘暴的源地在干旱和半干旱地区,由于大气环流的作用,影响到下风向的半湿润甚至湿润地区。无论何地干旱、半干旱地区都将存在沙尘暴发生的自然条件,而其下风向必将受到不同程度的影响,只是因为中国的季风气候,决定西北干旱、半干旱地区发生的沙尘暴必然影响东南部地区。在现有的科学技术条件下,人类所能做的就是调节自身的行为。因此,在沙尘暴源地实施生态建设是减缓沙尘暴发生的最重要措施,也是消除东部城市沙尘天气的主要途径。根据生态地理区域的特征,沙尘暴源地的干旱区、半干? 相似文献
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