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21.
为实现食用菌产业可持续发展,分析食用菌企业财务管理与成本控制的问题,并通过对食用菌种植成本的控制,达到企业资金的投入获得保障收益的稳定。从食用菌企业内部财务问题与生产投入着手,分析现阶段存在的问题及提出解决建议,确保食用菌企业内部利益上升的同时,提升企业整体实力及市场竞争力,确保食用菌产业健康稳步的发展。 相似文献
22.
为了进一步提高对芋疫病预测预报,科学指导生产上的防治,应用最小二乘法、频次分布、聚集度指标、m*-m回归分析和Taylor幂法则等对病株的空间分布型进行了分析。结果表明:当田间芋疫病病株率在0.427~0.513时,病株田间分布属聚集分布;当田间芋疫病病株率在0.720~0.820时,病株田间分布属均匀分布。此外其病株空间分布的基本成分是个体群,病株个体间相互吸引,病株在大田中存在明显的发病中心,且病株个体的空间格局随着病株密度的提高越趋均匀分。在此基础上,提出了Iwao最适理论抽样模型N=232.3783/m-87.9438,并建立序贯抽样模型T0(N)=0.3689N±1.7177$\sqrt{N}$,即:调查株数N时,若累计病株率超过上界可定为防治对象田,若累计病株率未达到下界时,可定为不防治田,若累计病株率在上下界之间,则应继续调查,直到最大样本数m0=0.3689时,也即病株率15%,所需抽样数542株止。 相似文献
23.
为了深入了解南海上层海洋热力状态的变化规律,利用1980—2015年共36年GODAS月平均海温资料,将5~366 m的垂直平均海温表征南海地区海洋上层的热含量,分析了南海海洋上层热状态的水平和垂直分布特征以及季节和年际变化特征。结果表明:年平均南海热含量水平分布表现为东高西低的形势,垂直纬向平均分布表现为暖水厚度和温跃层深度东厚(深)西薄(浅),垂直经向平均表现为暖水厚度南厚北薄,温跃层深度中间浅两边深;南海地区海温变化幅度在75~200 m处最大,不同深度海温距平均具有明显的年际和年代际变化特征;南海区域平均热含量在秋季最高,春夏次之,冬季最低,其年际变化明显,且在1998年之后出现明显的突变,由负值转变为正值,表现出明显的增温趋势;热含量季节EOF主模态空间分布形势表现为东高西低的特征,对应的时间序列在20世纪90年代末存在年代际转折,由主要为负值转化为主要为正值,表现在空间分布上,则为南海地区热含量由西高东低型转化为东高西低型。 相似文献
24.
华北地区夏玉米生产中磷素利用特征研究 总被引:3,自引:0,他引:3
为评估当前中国华北地区夏玉米生产中的磷素利用效率和影响因素,促进磷肥资源高效利用和降低损失和污染,本研究通过收集1980年以来公开发表的夏玉米田间试验的文献,对华北地区夏玉米磷肥试验数据进行收集、整理和分析,获得了夏玉米的籽粒与秸秆产量及其比例,以及施磷量与籽粒和秸秆磷含量的关系模型。研究发现,随着施磷量的增加,土壤-夏玉米作物系统的磷素表观盈亏量呈线性增加,在施磷达到75 kg/hm 2时,磷素表观盈亏量为0。华北地区的夏玉米磷肥平均利用效率约为15%;增加氮肥施用量以及与磷合理配施有利于提高磷肥利用效率。整体上,夏玉米对磷酸二铵的利用效率高于过磷酸钙;有机肥和化肥配施可以有效提高磷肥利用效率。夏玉米‘天泰60’品种的磷肥利用效率最高。在华北地区夏玉米生产中,选用磷酸二铵以及适合的氮肥水平、有机肥与化肥配施,可以提高磷肥利用效率,降低磷肥损失和环境污染风险。 相似文献
25.
26.
AIM: To investigate the effect and potential mechanism of microRNA-181a (miR-181a) on cigarette smoke extract (CSE)-induced the productions of pro-inflammatory factors and the expression of collagen IV, fibronectin and α-smooth muscle actin (α-SMA) in human bronchial epithelial cells (HBECs). METHODS: CSE-induced miR-181a expression was detected by RT-qPCR in the HBECs. After tansfected with miR-181a mimic, the releases of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and transforming growth factor-β1 (TGF-β1) were measured by ELISA, the protein expression of collagen IV, fibronectin and α-SMA was determined by Western blot. The activation of NF-κB/TGF-β1/Smad3 pathway was also evaluated by Western blot. RESULTS: CSE increased the levels of TNF-α, IL-1β, IL-6 and TGF-β1 and the expression of collagen IV, fibronectin and α-SMA, and decreased the expression of miR-181a in the HBECs (P<0.05). However, transfected with miR-181a mimic partially prevented the releases of TNF-α, IL-1β, IL-6 and TGF-β1, and inhibited the expression of collagen IV, fibronectin and α-SMA (P<0.05). Additionally, the activation of NF-κB/TGF-β1/Smad3 evoked by CSE was attenuated after transfected with miR-181a mimic. CONCLUSION: Up-regulation of miR-181a prevents the releases of CSE-induced pro-inflammatory factors and expression of collagen IV, fibronectin and α-SMA in the HBECs, and its mechanism may be related to the inhibition of NF-κB/TGF-β1/Smad3 pathway. 相似文献
27.
AIM: To investigate the role of microRNA-29b (miR-29b)-mediated TGF-β/Smad signaling pathway in the activation of hepatic stellate cells (HSC) and its effect on the progression of hepatic fibrosis in rats.METHODS: Hepatic liver fibrosis rat model was established, and its HSC were isolated. Normal rat HSC were also obtained and identified in vitro. RT-qPCR and Western blot were used to detect the alterations of miR-29b, TGF-β/Smad signaling pathway-related proteins and liver fibrosis marker proteins in the acquired cells. Finally, the direct targeting binding of miR-29b to TGF-β1 was identified by dual-luciferase reporter assay system.RESULTS: With the activation of HSC, the expression of miR-29b gradually decreased (P<0.01), while the expression of collagen type I and α-smooth muscle actin gradually increased (P<0.01). At the same time, the expression of Smad2/3/4 was significantly increased, and the expression of Smad7 was significantly decreased (P<0.01). Dual-luciferase reporter assay showed that miR-29b bound directly to "UCUCUCCGU" in the 3'UTR of TGF-β1, indicating that TGF-β1 was a downstream target gene of miR-29b.CONCLUSION: miR-29b may be involved in the inhibition of HSC activation and migration, thereby inhibiting the process of liver fibrosis. The biological function of miR-29b may be through the direct targeting of TGF-β1, thus regulating and inhibiting the TGF-β/Smad signaling pathway. 相似文献
28.
从粮食作物、经济作物及饲草的种植,饲草料的加工调制与利用,全舍饲肉羊的养殖及杂交繁育,以及羊粪尿的资源化利用等方面介绍了豫北山区“粮—草—羊”高效平衡养羊模式发展现状,以期为促进豫北山区资源可持续利用、山区生态环境良性循环和社会经济可持续发展提供思路。 相似文献
29.
PPARγ mediates effects of diosgenin on proliferation and apoptosis in human glioblastoma U87MG cells
AIM:To investigate the effect of diosgenin (Dio) on the proliferation, apoptosis and expression of peroxisome proliferator-activated receptor γ (PPARγ) in human glioblastoma U87MG cells and its possible mechanism. METHODS:Human astrocytes (HA) and U87MG cells were cultured in vitro and treated with Dio (0, 10, 20, 30, 40 and 50 μmol/L) and GW9662 (5 μmol/L) for 48 h, and then the cell viability was detected by CCK-8 assay. Cell colony formation assay was used to assess the proliferation potential. Flow cytometry was used to analyze the cell cycle distribution and apoptosis. The mRNA expression level of PPARγ was measured by RT-PCR. Western blot was used to determine the protein levels of PPARγ, cyclin D1, cyclin E1, Bcl-2 and Bax. RESULTS:Dio had no significant influence on the viabi-lity of HA (P>0.05). However, Dio remarkably reduced the viability of U87MG cells in a dose-dependent manner (P<0.05) with IC50 of 24.31 μmol/L. Meanwhile, Dio remarkably diminished colony formation ability (P<0.05), induced G0/G1 phase arrest of the cell cycle and apoptosis (P<0.05), up-regulated the expression of PPARγ at mRNA and protein levels, increased the protein level of Bax (P<0.05), and down-regulated the protein levels of cyclin D1, cyclin E1 and Bcl-2 (P<0.05) in a dose-dependent manner. However, these effects induced by Dio were inhibited by GW9662 (P<0.05), a specific inhibitor of PPARγ. CONCLUSION:Dio may inhibit proliferation and induce apoptosis in human glioblastoma U87MG cells most likely via up-regulating the expression of PPARγ, and then down-regulating the protein levels of cyclin D1, cyclin E1 and Bcl-2, and up-regulating the protein level of Bax. 相似文献
30.