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61.
玉米霜霉病的侵染途径及防治措施   总被引:1,自引:0,他引:1  
系统综述了玉米霜霉病的症状表现、发生规律和防治措施等方面的研究进展.加强进境植物检疫、及时清除病残体和选育高抗的玉米品种是防治玉米霜霉病的重中之重.  相似文献   
62.
张勇  孙璀 《动物营养学报》2011,23(4):536-541
钙调磷酸酶-活化T细胞核因子(nuclear factor of activated T cells,NFAT)信号途径作为肌肉细胞内重要的生物信号转导途径,在肌肉细胞中起到调节枢纽的作用,与肌肉生长及肌纤维的类型有密切关系.而肌肉组织降解在动物肌肉嫩化过程中具有重要的意义.因此,钙调磷酸酶-NFAT信号途径可能与肌肉...  相似文献   
63.
卵泡从原始卵泡发育为成熟卵泡,直至排卵、黄体发育等过程都受到精密的调控,产生大量的优势卵泡是绵羊产多羔及实现快速扩繁的关键因素。研究发现,相关信号通路和转录因子通过影响绵羊卵泡中卵母细胞、颗粒细胞的生长,进而调控卵泡的发育成熟,对这些信号通路进行深入了解,有助于探索卵泡发育的调控机制,早日实现绵羊高效繁育。Notch是卵泡发育过程中发挥重要作用的高度保守信号通路,PI3K/AKT/mTOR信号通路各成员都是广泛存在于细胞内的信号转导分子,在卵泡发育早期发挥了主要作用,还有间隙连接(gap junction,GJ)和跨带突触(transzonal projections,TZPs)等物理连接方式,在细胞间的交流通讯起到重要作用。作者详细介绍了Notch信号通路、PI3K/AKT/mTOR信号通路、间隙连接及跨带突触的结构功能在绵羊卵泡发育中的调控作用,为进一步探明绵羊卵泡发育的调控机制提供参考。  相似文献   
64.
乳腺癌是犬、猫等伴侣动物与人类常发疾病,作为人类及动物常患恶性肿瘤和主要致死肿瘤之一,其疾病负担仍呈逐步加重趋势,乳腺癌的预防及治疗形势愈加严峻。上皮间质转化(EMT)是乳腺癌发生发展中重要的生物学过程。EMT还可促进恶性肿瘤的侵袭、扩散及耐药,因此它在肿瘤的研究中日益受到关注,靶向于EMT是治疗乳腺癌的重要研究方向与热点。文章就EMT发生过程中细胞形态功能及标志物的变化、EMT分类及EMT与乳腺癌的关系分别展开论述,详细解析了EMT相关TGF-β/Smad、NF-κB及Wnt信号通路转导途径;随后对乳腺癌治疗药物研究进展,包括TGF-β/Smad通路抑制剂开发,相关药物、基因及细胞因子治疗前景、NF-κB通路与Wnt通路抑制剂的动物试验研究结果进行了详细论述;最后对乳腺癌的治疗发展与趋势进行了展望。深入认识信号通路调控乳腺癌EMT的生物学过程,明确其发生发展机制,寻找关键靶点及开发靶向药物,将为乳腺癌的精准治疗带来曙光。  相似文献   
65.
66.
Juvenile hormone (JH) is an insect-specific hormone that regulates molting and metamorphosis. Hence, JH signaling inhibitors (JHSIs) and activators (JHSAs) can be used as effective insect growth regulators (IGRs) for pest management. In our previous study, we established a high-throughput screening (HTS) system for exploration of novel JHSIs and JHSAs using a Bombyx mori cell line (BmN_JF&AR cells) and succeeded in identifying novel JHSIs from a chemical library. Here, we searched for novel JHSAs using this system. The four-step HTS yielded 10 compounds as candidate JHSAs; some of these compounds showed novel basic structures, whereas the others were composed of a 4-phenoxyphenoxymethyl skeleton, the basic structure of several existing JH analogs (pyriproxyfen and fenoxycarb). Topical application of seven compounds to B. mori larvae significantly prolonged the larval period, suggesting that the identified JHSAs may be promising IGRs targeting the JH signaling pathway.  相似文献   
67.
AIM: To investigate the effect of paricalcitol (P) on renal tubulointerstitial fibrosis and the underlying mechanisms in diabetic nephropathy (DN).METHODS: DN rat model was induced by a single intraperitoneal injection of streptozotocin after fasting. The animals were randomly divided into 2 groups:the DN rats in paricalcitol-intervened group (group P) were injected intraperitoneally with paricalcitol dissolved in propylene glycol after the day when the model was induced successfully at a dose of 0.4 μg/kg (3 times a week); the DN rats in DN group (group D) were given isopyknic propylene glycol. Normal control group (group C) was also set up. The samples of blood, urine and renal tissue were collected after intervention of paricalcitol for 12 weeks. The biochemical indexes were measured. The renal tissues were used for pathologic observation and determining the expression of transforming growth factor-β1 (TGF-β1), Wnt-4, β-catenin and Klotho by immunohistochemistry and Western blotting. In addition, the correlation among the above indexes was analyzed.RESULTS: (1) Scr, BUN and 24 h urine protein increased significantly in group D compared with group C, while decreased in group P compared with group D (P<0.05). (2) The area of renal tubulointerstitial fibrosis increased in group D compared with group C, while decreased in group P compared with group D (P<0.05). (3) The expression of Klotho decreased, while the expression of TGF-β1, Wnt-4 and β-catenin increased in group D compared with group C (P<0.05). Compared with group D, the expression of Klotho increased, while the expression of TGF-β1, Wnt-4 and β-catenin decreased in group P (P<0.05). (4) The expression of Klotho was negatively correlated with the fibrosis area, TGF-β1, Wnt-4 and β-catenin (P<0.05).CONCLUSION: Paricalcitol inhibits renal tubulointerstitial fibrosis in DN by promoting the expression of renal Klotho, and inhibiting Wnt/β-catenin signaling pathway activation and TGF-β1 synthesis.  相似文献   
68.
AIM: To explore the effect of tanshinone ⅡA on human osteosarcoma HOS cells and the underlying mechanism.METHODS: The cell viability and the appropriate dose of tanshinone ⅡA were determined by CCK-8 assay. Colony formation assay and Transwell assay were used to investigate the proliferation and migration abilities of the HOS cells treated with tanshinone ⅡA. The apoptosis of the HOS cells was monitored by Hoechst 33258 staining, transmission electron microscopy and flow cytometry. The protein levels of apoptosis-related molecules and JNK signaling-associated proteins were determined by Western blot. Meanwhile, a JNK inhibitor was added for confirming the relationship between the pathway and apoptosis mentioned above.RESULTS: Tanshinone ⅡA inhibited both HOS cell proliferation and migration in a dose-and time-dependent manner. Exposure of the HOS cells to tanshinone ⅡA resulted in the activation of apoptosis. Tanshinone ⅡA treatment increased the protein levels of cleaved caspase-3, Bax and JNK signaling-associated proteins, and decreased the protein level of Bcl-2, which were reversed by JNK inhibitor SP600125. Moreover, the result of CCK-8 assay revealed that tanshinone ⅡA-induced cell death was alleviated by JNK inhibitor.CONCLUSION: Tanshinone ⅡA induces cell growth inhibition and the activation of apoptosis via JNK signaling pathway in human osteosarcoma HOS cells.  相似文献   
69.
为研究几种经济红藻中茉莉酸合成途径的关键物质,实验采用液相色谱—质谱联用技术(LC-MS)对茉莉酸生物合成途径相关物质建立检测方法,并对龙须菜、坛紫菜受到机械损伤时各物质的变化情况进行检测。以100%甲醇提取茉莉酸(JA)、茉莉酸甲酯(MeJA)、12-氧-植物二烯酸(12-OPDA)和13-氢过氧化亚麻酸(13-HpOTE),利用XBridge TM C18色谱柱,以甲醇/水为流动相分离4种物质。优化条件下4种物质得到良好分离,加标回收率为81.23%~90.25%,检测限为0.04~0.56 ng/mL,灵敏度高。坛紫菜、龙须菜和真江蓠3种红藻中,坛紫菜中未检测到JA和13-HpOTE,4种物质均在另外2种藻中检测到。龙须菜受机械损伤胁迫后,4种物质在短时间内得到积累,其中13-HpOTE响应迅速。研究表明,红藻中可能存在类似于植物的茉莉酸合成途径,并参与对损伤的胁迫响应。  相似文献   
70.
AIM:To investigate the effect of CUDC-907, a dual histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K) inhibitor, on the DNA damage, cell cycle distribution and autophagy in human glioma U251 cells. METHODS:U251 cells were treated with CUDC-907 of different concentrations, and the cell viability was detected by MTT assay. The quantitative γ-H2AX foci were determined by laser scanning confocal microscopy. The cell cycle distribution of U251 cells was examined by flow cytometry. The protein expression was determined by Western blot analysis. RESULTS:CUDC-907 inhibited the cell viability and the phosphorylation of Akt and p70 ribosomal protein S6 kinase (p70s6K) in the U251 cells (P<0.05). In CUDC-907-treated cells, the number of γ-H2AX foci and protein expression of γ-H2AX were increased significantly (P<0.05). CUDC-907 also induced cell arrest in the G2/M phase by up-regulating the expression of p21, and inhibiting the protein level of cyclin B1 and the phosphorylation of cell division cycle protein 2 (Cdc2). In addition, CUDC-907 triggered cell autophagy, and inhibition of autophagy increased CUDC-907-induced DNA damage of U251 cells. CONCLUSION:CUDC-907 significantly inhibits PI3K/Akt signaling pathway, induces DNA damage and arrests cell cycle in G2/M phase. Blockage of autophagy promotes CUDC-907-induced DNA damage of U251 cells.  相似文献   
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