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151.
从健康桑树根系中分离筛选得到一株内生产油脂真菌——菜豆壳球孢菌MOD-1(Macrophomina phaseolina,MOD-1)。结合均匀设计和单因子筛选法得到该菌株产油脂发酵培养基最优配方为:可溶性淀粉105 g/L,蛋白胨1.1 g/L,磷酸二氢钾1.5 g/L,硫酸铵0.3 g/L,硫酸镁0.32 g/L,氯化锰4.9 nmol/L。在此基础上优化该菌株产油脂的摇瓶发酵条件为:发酵液初始pH7.0,发酵温度26℃,摇瓶转速190 r/min,装液量100 mL。在优化后的培养基组分及摇瓶发酵条件下培养6 d,菌体生长量(干质量)高达41.852 g/L,油脂产量达到25.511 g/L。利用气相色谱-质谱法分别测定菌株在优化后的培养基或发酵条件下产生油脂的脂肪酸组成,前一种条件下检测出9种脂肪酸成分,其中单不饱和脂肪酸含量为67.92%;后一种条件下检测出7种脂肪酸成分,其中单不饱和脂肪酸含量为74.32%。结果表明,在优化培养基及摇瓶发酵条件下,MOD-1菌株的油脂产量增高,组成简单,易于纯化,且单不饱和脂肪酸含量较高。 相似文献
152.
AIM:To observe whether selective inhibition of endothelin receptor A (ETRA) improves white matter lesions (WMLs), and explore the mechanism. METHODS:Sprague-Dawley rats (n=33) were randomly divided into sham operation group (n=9), treatment group[stroke-prone renovascular hypertensive rats-modified 2 vessel occlusion (RHRSP-modified 2VO) + ambrisentan (n=12)] and placebo group[RHRSP-modified 2VO + vehicle (n=12)]. Drug and vehicle administration was performed from 17th to 20th week and monitoring of systolic arterial pressure was performed weekly. Morris water maze test was conducted to evaluate the function of cognition. The protein levels of endothelin-1 (ET-1) in the cortex, corpus callosum and caudate putamen were quantitatively analyzed respectively. The severity of WMLs and the relationship between ET-1 and vessels were observed by the method of histopathology. RESULTS:The difference of systolic arterial pressure between treatment group and placebo group was not significant. The animals in treatment group exhibited shorter escape latency (P<0.05), more times of crossing platform (P<0.05), lower level of ET-1 in corpus callosum and caudate putamen (P<0.05), respectively, improved WMLs severity (P<0.05) and lower binding level of ET-1 to vessels compared with the placebo group. CONCLUSION:Selective inhibition of endothelin receptor A improves the severity of WMLs and ameliorates the cognitive function. 相似文献
153.
黄色镰刀菌Fusarium culmorum为黑龙江省马铃薯干腐病主要致病菌,干腐病可以导致马铃薯在窖藏过程中发生腐烂,影响薯块的商品价值和食用价值,为进一步研究马铃薯干腐病的发生和防治,本研究采用黄色镰刀菌对不同抗性的马铃薯块茎进行侵染,对病原菌侵染过程中薯块的抗氧化酶及细胞壁降解酶变化及病程相关基因的表特性进行了研究。结果表明,当黄色镰刀菌侵染块茎时,块茎中的可溶性蛋白和丙二醛(malondlaldehyde,MDA)含量,超氧化物歧化酶(superoxide dismutase,SOD)、过氧化物酶(peroxidase,POD)活性、几丁质酶(chitinase)和β-1,3-葡聚糖酶(β-1,3-glucanase)活性都呈现不同程度的上升趋势。非特异性脂质转移蛋白基因StLTPa1表达量随着黄色镰刀菌的侵染时间呈波动性,在植物防御反应中发挥一定的作用。 相似文献
154.
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157.
京脆1 号是由两个自交不亲和系05132 和05177 配制而成的鲜食水果型萝卜一代杂种。生长期75~80 d(天),叶
片近板叶型,深绿色,半直立株型。肉质根椭圆形,尾根细,茎盘小。根长13 cm,横径12 cm,平均单根质量1.2 kg,每
667 m2 产量5 000~6 000 kg。肉质根3/4 露出地面,出土部分浅绿色,入土部分白色,肉色浅绿,肉质甜脆,VC 含量 380
mg·kg-1(FW),硫苷含量318.8 μmol·kg-1(FW),适合生食。田间对病毒病和软腐病的抗性强于对照满堂红。适合北京、
天津、河北、山东等地种植。 相似文献
158.
AIM: To explore the effects and mechanism of eleutheroside (ETS) B or E on the proliferation of HBZY-1 cells treated with high glucose. METHODS: The HBZY-1 cells were cultured under high glucose condition. The 4th generation of HBZY-1 cells was used for determining the optimal cell density, which was consistent with the growth regulation curve of the cells. The cells were divided into 6 groups: low glucose (LG) group, high glucose (HG) group, high glucose plus ETS-B/E (low dose, medium dose and high dose) groups, and high glucose plus losartan (LTG) group. After all cells were treated with the corresponding drugs at 24 h, 48 h and 72 h, the inhibitory rate of the proliferation was measured, and the expression of TGF-β1 and PPARγ was detected by immunocytochemistry and Western blotting. RESULTS: The best cell density was 2 000 cells/well, which was complied with the basic rules of the cell growth, and high glucose significantly promoted the HBZY-1 cell proliferation. At each time point, the inhibitory effects of ETS-B/E were significantly different between HG group and LTG group on the proliferation of the HBZY-1 cells (P<0.05). The expression of TGF-β1 was significantly inhibited, and the expression of PPARγ was significantly promoted by ETS-B/E (P<0.05). ETS-E showed stronger effect than ETS-B (P<0.05) in a concentration- and time-dependent manner. CONCLUSION: ETS-B/E significantly inhibits the proliferation of HBZY-1 cells under high glucose condition by decreasing TGF-β1 expression and promoting PPARγ expression. 相似文献
159.
160.