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排序方式: 共有98条查询结果,搜索用时 31 毫秒
41.
AIM: To explore the mechanism of propolis on the inhibition of atherosclerosis and thrombosis in injured human umbilical vascular endothelial cells (HUVECs) induced by tumor necrosis factor alpha (TNF-α)in vitro.METHODS: TNF-α at the concentration of 50 μg/L was used to induce the injury of HUVECs. The injured HUVECs were treated with water extract propolis (WEP) at the concentrations of 50, 100 and 200 mg/L for 6 h, 12 h and 24 h. The expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was examined by flow cytometry.RESULTS: The expression of ICAM-1 and VCAM-1 was significantly higher in injured HUVECs (P<0.01) than that in the control cells. The expression of ICAM-1 and VCAM-1 was downregulated by WEP treatment in a dose-dependent manner. Between the groups of 100 and 200 mg/L WEP, the difference was significant. In the injured HUVECs treated with 50 mg/L WEP, the inhibitory effect on the expression of ICAM-1 and VCAM-1 was presented in a time-dependent manner. Compared to the single administration, the use of WEP combined with fluvastatin showed better inhibitory effect on the expression of ICAM-1 and VCAM-1 in the injured HUVECs induced by TNF-α (P<0.01).CONCLUSION: WEP may be helpful for the protection of vascular endothelial cells by inhibiting the expression of ICAM-1 and VCAM-1 in a time-and dose-dependent manner. The protective effect of WEP on endothelial cells may be synergic with the inhibitor of HMG-CoA reductase such as fluvastatin sodium. 相似文献
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基于扩张状态观测器的路面附着系数实时估计 总被引:2,自引:0,他引:2
对车辆动力学控制中的道路路面附着系数实时估计问题进行研究.首先使用魔术公式建立1/4车辆制动模型,即车轮制动动力学模型;然后将其中的附着系数相关项视为制动系统的扩张状态,建立其扩张状态观测器,通过轮速信号和制动力矩信号实时观测制动过程中地面与轮胎间的纵向力,进而计算出路面附着系数;最后在均匀路面和突变路面条件下进行仿真研究.结果表明,所提出的方法对车辆制动系统参数摄动和传感器噪声具有鲁棒性,可以准确地实现道路路面附着系数的实时估计,观测器与控制器设计具有一定独立性. 相似文献
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《Wood material science & engineering》2013,8(3-4):98-104
Abstract End-grain surfaces of spruce wood specimens that were planed with a microtome knife were chemically modified by treatment with bleaching reagents, namely sodium hypochlorite and peracetic acid, and the effect of the surface modification on bond strength of end-grain joints was studied. The chemically treated samples were compared with sawn surfaces, microtome-planed specimens that were additionally irradiated by light, and surfaces that were solely planed with a microtome knife. Significantly higher bond strength compared with the microtome-planed specimens was observed for the sawn specimens and for hypochlorite-modified samples. These findings were ascribed on the one hand to an increased surface roughness resulting from the mechanical process of sawing leading to an enlargement of the bonding area. On the other hand, during the etching process with sodium hypochlorite a pulp of cell walls and cell wall fragments was formed, leading to a partially closed surface which prevented overpenetration of adhesive into the opened cells. 相似文献
44.
《Wood material science & engineering》2013,8(2):90-95
Abstract In a previous study it was shown that the mechanical stability of an end-grain joint bonded with a one-component polyurethane adhesive (PUR) was insufficient compared with melamine–urea–formaldehyde and phenol–resorcinol–formaldehyde bonding. Based on this, the aim of this study was to improve the mechanical stability of the end-grain joint by means of a hydroxymethylated resorcinol (HMR) primer and by increasing the spreading quantity. To study the effect of HMR and the increased spreading quantity on the adhesive bond strength of end-grain to end-grain-bonded wood samples, three-part Norway spruce wood specimens were tested in tension. Before bonding, each end-grain surface was treated with an aqueous solution of HMR. The two axially orientated outer parts of the specimens were jointed with the middle part using a PUR adhesive. Compared with untreated, i.e. non-primed samples, the tensile strength of HMR-treated specimens was more than doubled. Furthermore, a positive effect of increased adhesive spread was shown for untreated PUR-bonded samples. An increase in adhesive spread by a factor of 1.6 led to an improvement in tensile strength by a factor of about 2.6. 相似文献
45.
采用PCR方法扩增嗜水气单胞菌(Aeromonas hydrophila)外膜蛋白相关基因,即粘附素(Aha)、外膜蛋白A(OmpA)基因全长序列,进行DNA测序及生物信息学分析。结果表明:Aha基因长1 314 bp,推导编码355 aa,5~24 aa区域为跨膜螺旋,26~355 aa区域为革兰氏阴性菌孔蛋白结构域(PF00267),Aha蛋白三级结构与模板(PDB:1PHO_A)相似性达28.21%;OmpA基因长1 102 bp,推导编码338 aa,含有OmpA跨膜结构域(PF01389)和OmpA结构域(PF00691),预测OmpA蛋白抗原表位位于64~69 aa、160~171 aa、244~249 aa、259~274 aa和295~301 aa区域,OmpA蛋白三级结构OmpA跨膜结构域和OmpA结构域与模板(PDB:1BXW_A,PDB:4ERH_A)相似性分别为27.45%和57.58%;进一步采用拉马钱德兰图(Ramachandran plot)检测分析,与Aha、OmpA基因蛋白三级结构预测结果一致。本研究有助于理解嗜水气单胞菌致病的分子机制,为鱼类疾病防治及疫苗应用提供科学参考。 相似文献
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目的探讨蛋白激酶C抑制剂对吸烟大鼠脑血管内皮细胞细胞间粘附分子1蛋白和mRNA表达的影响。方法无脑梗死大鼠18只,随机分为不吸烟组6只、吸烟组6只和吸烟蛋白激酶C抑制剂组6只。脑梗死大鼠48只,随机分为脑梗死组24只和蛋白激酶C抑制剂组24只,分别于梗死后2、6、12及24h干预,每个时间点6只。采用免疫组织化学法和原位杂交法分别测定细胞间粘附分子1蛋白和mRNA。结果吸烟大鼠脑血管内皮细胞细胞间粘附分子1蛋白和mRNA均有表达,吸烟蛋白激酶C抑制剂组脑血管内皮细胞细胞间粘附分子1蛋白和mRNA的表达明显低于吸烟组(P<0.05)。蛋白激酶C抑制剂组细胞间粘附分子1蛋白和mRNA的表达均低于对应时间点脑梗死组(P<0.05),且梗死后2h蛋白激酶C抑制剂组细胞间粘附分子1蛋白和mRNA的表达明显低于其他时间点组。结论蛋白激酶C抑制剂可阻断吸烟大鼠脑血管内皮细胞细胞间粘附分子1蛋白和mRNA表达,并且早期用药效果可能更好。 相似文献