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排序方式: 共有513条查询结果,搜索用时 921 毫秒
41.
LI Wei CAO Ji ZHOU Ling-li LUO Wang YANG Chun LUO Cheng-piao LI Yuan SU Jian-jia 《园艺学报》2014,30(12):2142-2147
AIM: To investigate the effect of silencing cell division cycle 25a (CDC25a) gene on the proliferation of human hepatoma HepG2 cells. METHODS: CDC25agene in human hepatoma HepG2 cells was silenced by RNA interference. Real-time PCR was applied to detect the expression of CDC25a, cyclin E and CDK2 at mRNA levels in the HepG2 cells. Western blotting was applied to detect the expression of CDC25a at protein level. In addition, MTT assay, Giemsa staining and flow cytometry were used to measure the proliferation of human hepatoma HepG2 cells. RESULTS: The expression of CDC25a at mRNA and protein levels in RNA silence group was lower than those in negative control group and normal control group (P<0.05). The mRNA expression of cyclin E and CDK2 in silence group was lower than that in negative control group and normal control group (P<0.05). The cell proliferation in silence group was lower than that in negative control group and normal control group (P<0.05). The results of flow cytometry revealed that the cells in silence group were blocked in G1 phase. CONCLUSION: Infection of LV-CDC25a-RNAi recombinant to the HepG2 cells effectively inhibits the CDC25agene expression and the proliferation of human hepatoma cells, and arrests the cells in G1 phase, suggesting that CDC25agene may be a key target for the treatment of liver cancer. 相似文献
42.
观察3种方法治疗雏鹅病毒性肝炎的疗效,选出较好的治疗方案,以提高雏鹅病毒性肝炎的治愈率。分别进行人工感染预防及治疗试验和临床治疗试验。在临床治疗试验中选自然发病的莱茵雏鹅共5466只,将患鹅随机分为4组,分别采用保肝散、病毒灵、保肝散加病毒灵治疗,并设空白对照组。结果表明,保肝散配合病毒灵组治疗效果最好,治愈率达96.05%;保肝散组次之,为77.97%;病毒灵组再次,为72.18%;对照组为14.72%。采用保肝散配合病毒灵组治疗雏鹅病毒性肝炎高于其他两种方法,为临床治疗该病提供了确实可行的治疗方法。 相似文献
43.
研究了在重金属镉胁迫条件下,大弹涂鱼(Boleophthalmuspectinirostris)肝脏黄嘌呤氧化酶活性的变化。重金属镉胁迫12h时0·5mg/LCd2 组XOD酶活性和对照组比较显著升高(P<0·05);胁迫24h时,大弹涂鱼0·05mg/LCd2 组肝脏的XOD酶活性和对照组比较极显著升高(P<0·01),而0·5mg/LCd2 组酶活性结果却降低;恢复3d时0·5mg/LCd2 又极显著升高(P<0·01)。在镉胁迫解除5d时,3个浓度组的酶活性均极显著降低(P<0·01),其中0·05mg/LCd2 组和0·5mg/LCd2 组的酶活性和对照组酶活性比较无显著差异(P>0·05),5mg/LCd2 组的酶活性极显著低于对照组的酶活性(P<0·01)。实验结果表明,大弹涂鱼肝脏黄嘌呤氧化酶活性对水体中镉污染敏感,有可能用做海洋环境污染的生物标记。 相似文献
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46.
鸡肝组织中磺胺类药物多残留分析法 总被引:26,自引:0,他引:26
建立了鸡肝组织中磺胺嘧啶、磺胺二甲基嘧啶、磺胺甲氧吡嗪、磺胺-6-甲氧嘧啶、磺胺甲恶唑、磺胺-2,6-二甲氧嘧啶和磺胺喹恶啉的多残留高效液相色谱分析法。样品经乙腈提取、正己烷液-液分配和碱性氧化铝柱固相萃取法净化后用反相高效液相色谱法测定(UV270nm)。7种磺胺类药物标准曲线的相关系数(r^2)为0.9991-1.0000(0.01μg/ml-0.5μg/ml)。在0.05mg/kg-0.5mg/kg浓度范围内,磺胺类药物的回收率为68.8%-100.0%,变异系数为1.3%-12.0%。 检测限为0.01mg/kg-0.03mg/kg,定量限低于0.05mg/kg。 相似文献
47.
To demonstrate the distribution and expression of heat shock proteins (HSPs) in the liver, five kinds of HSPs, namely HSP70 , HSP72, HSP86, HSP90 and HSP27 were determined after a long distance transport using immunohistochemistry and Western blot. All five HSPs were regularly detected in the liver of both the transported and the control group. Both nuclear and cytoplasmic labeling was present in hepatic cells;however, localization of HSPs was quite different in hepatocytes. The majority of HSP70, HSP72 and HSP27appeared to predominate in cytoplasm of the hepatocytes. Nuclear signals of HSP90 and HSP86 were most prominent in hepatocytes in which immunostaining in the cytoplasm was relatively weak compared with that in the nucleus. There was subjectively lower staining in the edge of hepatic labule, and lower numbers of HSPs labeled hepatic cells corresponded to light microscopic lesions. The obvious inductions of some HSPs were detected in the liver, especially the HSP90(P< 0.01) which belongs to the HSP90 family. However, the obvious reductions of HSP86 (P < 0.05), which belong to the HSP90 family, and HSP27 ( P < 0.05), which belong to small families, were detected in stressed pig liver after six hours of long distance transportation. 相似文献
48.
猪肝脏组织表达序列标签(ESTs)的初步分析 总被引:4,自引:0,他引:4
构建了猪肝脏组织cDNA文库 ,并对文库中随机挑选的 4 38个克隆的表达序列标签 (ESTs)进行了研究。结果表明 ,在所研究的 4 38个ESTs中 ,186个在猪种中已有匹配序列 ,37个在人类及其它物种中可以找到同源序列 ,2 15个为未知功能基因。试验还测定了文库中 4 5个cDNA克隆的全长插入序列 ,结果表明 ,19个为已知功能基因 ,11个没有发现开放阅读框 ,其它 15个具有开放阅读框 ,但基因的功能未知。这些结果初步代表了肝脏组织的功能基因表达谱。 相似文献
49.
AIM: To investigate the protective role of heat-shock protein 70 (HSP70) in the pathogenesis of gastric mucosal damage in cirrhotic rats with portal hypertensive gastropathy (PHG).METHODS: The rat model of liver cirrhosis with PHG was established by injection with tetrachloride.The animals were divided into normal control group, PHG group, PHG+heat treatment group, PHG+BPI21 group and PHG+endotoxin groups.The endotoxin used in the experiment was at the dose of 3 mg/kg and endotoxin antagonist BPI21 was at the dose of 2 mg/kg.HSP70 was induced by pre-treating the animals with mild whole-body heating.The levels of HSP70 and tumor necrosis factor alpha (TNF-α) in the gastric mucosa were measured by ELISA.Furthermore, the pathological changes of the gastric mucosa were observed under microscope with HE staining.RESULTS: Compared with the normal control rats, the rats in PHG group showed obvious gastric pathological lesion, decrease in HSP70 production and increase in TNF-α level in the gastric mucosa, and increased endotoxin concentration in the plasma.Compared with PHG+endotoxin group, the gastric mucosal lesion in PHG+BPI21 group was significantly attenuated, accompanied by the increase in HSP70 production and decrease in TNF-α level in the gastric mucosa.Heat treatment increased HSP70 production and decreased TNF-α concentration in the PHG rats, thus attenuating the gastric mucosal damage.CONCLUSION: HSP70 alleviates the gastric mucosal lesion induced by endotoxin in cirrhotic rats with PHG and decreases the concentration of TNF-α in gastric mucosa, indicating a protective role of HSP70 in the pathogenesis of gastric mucosal damage in PHG. 相似文献
50.
Image-guided tumor thermal ablation plays a key role in the management of hepatocellular carcinoma. Thermal ablation for hepatic tumors not only generates directly killing effect on liver tumors, but also improves the level of anti-tumor immunity of the host. Thermal ablation potentially affects the anti-tumor immunity in the following ways: (1) causing necrosis that is a source for intracellular antigens, and also inducing local inflammation, which further stimulates the antigen-presenting cells; (2) removing the tumor burden; (3) undergoing the process of heat shock in surviving tissue, leading to increase in the expression of heat shock proteins; (4) activating and enhancing tumor-specific T-cell responses. This review discusses these possible mechanisms. 相似文献