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41.
1997年田间调查时,发现一种寄生于棉铃虫的微孢子虫,对棉铃虫具有很强的致病力。为明确环境因子对该微孢子虫及其致病力的影响,测定了温度与紫外线对该微孢子虫及其杀虫效果的影响。结果表明,该微孢子虫孢子耐受温度范围较宽,最高温度上限为55℃。温度对其致病力有显著影响,在一定温度范围内,随着生境温度的升高,微孢子虫对棉铃虫幼虫致病力增强。该微孢子虫对紫外线较敏感,在紫外线照射下易失活而丧失致病力。  相似文献   
42.
李明丽  鲁绍雄 《家畜生态》2004,25(4):241-244
猪胚胎死亡直接影响着母猪的产仔数,并进而影响着养猪生产的经济效益。因此,在深入研究猪胚胎死亡规律及其影响因素的基础上,通过有效的措施降低胚胎死亡率,对提高母猪窝产仔数和经济效益具有十分重要的意义。本文综述了影响猪胚胎死亡的遗传、环境、营养和疾病等因素,并对生产实践中如何通过综合预防措施降低猪胚胎死亡率进行了初步探讨。  相似文献   
43.
为了探索微波处理作为木质包装替代处理方法的可能性,对不同规格和含水量的杨树木块进行微波处理试验,结果表明:频率为2450MHz的微波能够穿透厚度为10cm的杨树木材;当微波功率为900W时,规格为10cm×10cm×10cm和10cm×10cm×2.5cm的新木块中黄斑星天牛(Anoplophora nobolis)幼虫完全死亡所需时间分别为5min和2min;而干木块中则仅需3min和30s.对微波处理引起木材温度变化和水分损失以及天牛幼虫的水分损失进行了初步研究.  相似文献   
44.
陇东黄土高原冬小麦生产农业气象要素分析   总被引:15,自引:7,他引:15  
对陇东黄土高原半湿润半干旱气候区旱地冬小麦生长期光、热、水三要素与产量进行了相关分析,得出对冬小麦产量起决定作用的农业气象要素为:孕穗—成熟期光照时数,≥0℃积温,开春土壤含水量 返青—孕穗期降水量(R2 3H)。建立了逐步回归方程,Y=-317.138 0.6317X1 0.4647X2。  相似文献   
45.
AIM: To explore the regulatory mechanism of nerve growth factor (NGF) on neurokinin A in the experimental asthmatic guinea pig. METHODS: Radioimmunoassay was used to determine the alteration of neurokinin A levels in the lower respiratory tract and visceral sensory afferent sites while NGF was absent (inhalation of NGF antibody through nasal cavity) in the asthmatic guinea pig. RESULTS: The contents of neurokinin A in the trachea, bronchus, lung, C7-T5 spinal ganglia and the correspondent spinal dorsal horn, nodose ganglia and solitary nucleus area in the experimental asthmatic guinea pig with the absent of NGF in the respiratory tract were much lower than those in the asthmatic and control groups (P<0.01). CONCLUSION: NGF upregulated the contents of neurokinin A in the lower respiratory tract and visceral sensory sites of the experimental asthmatic guinea pig, and both might be involved in the pathogenesis of asthma.  相似文献   
46.
47.
AIM: To examine the expression and distribution of tumor necrosis factor-α (TNF-α), tumor necrosis factor receptor I (TNFR I) and apoptosis in oral lichen planus, and evaluate their roles and relation in the oral lichen. METHODS: Immunohistochemical technique and TUNEL were employed to study the expression of TNF-α, TNFR I and apoptosis in 50 cases of oral lichen planus and 10 normal oral mucosa specimens. RESULTS: Compared with the normal control group, TNF-α expression was upregulated in mononuclear cells in lamina propria and decreased in keratinocytes in oral lichen planus lesion (P<0.05). On the contrary, TNFR I expression was increased in keratinocytes and decreased in lamina propria in oral lichen planus lesion (P<0.05). The increased apoptosis index in keratinocytes and the decreased apoptosis index in lamina propria were found in oral lichen planus (P<0.05). CONCLUSION: The accelerated apoptosis of keratinocytes and the inhibition of lymphocytes apoptosis may contribute to the formation and progression of oral lichen planus.  相似文献   
48.
AIM: To study the role of liver in immune regulation in experimental endotoxemia. METHODS: 17 castrated male goats were subjected to simultaneously installing catheters in jugular, hepatic and portal veins by surgery. Four days later, lipopolysaccharide (LPS) was infused in term of three groups as followings: In group ①, LPS of 20 EU (endotoxin unit, EU)·kg-1 was infused into portal vein; In group ②, LPS of 20 EU·kg-1 was infused into jugular vein and LPS of 1 500 EU·kg-1 infused into jugular vein in group ③. Before and after infusion, blood samples were collected from the three veins through the catheters for 8 h.The plasma levels of TNF-α were measured by RIA. RESULTS: In group ①, the plasma TNF-α levels of hepatic and portal vein rose to peak value at 5 h, but that of the jugular vein did not changed. In group ②, the plasma TNF-α levels in hepatic vein rose to peak value at 3 h. The TNF-α levels of jugular vein rose to peak value at 1 h and the one in portal vein enhanced continuously between 0-8 h. In group ③, the plasma TNF-α levels in jugular, hepatic and portal vein rose to significant peaks at 1 h simultaneously. CONCLUSION: During experimental endotoxemia,liver showed different dynamic characteristics in TNF-α secretion according to the pathway and doses of LPS delivery.  相似文献   
49.
AIM: To investigate inhibition of K562 cell growth by antisense drug targeted VEGF mRNA. METHODS: X7, 20-mer antisense sequences were selected, synthesized and modified with phosphorothioate. The drug was transfected into K562 cells in the present of lipofection. Cell growth was assayed by trypan blue dye exclusion assay and MTT. The level of VEGF protein in the media was determined by ELISA. The morphology of apoptotic cells were observed by Giemsa staining, and the propotion of apoptotic cells was detected by flow cytometry. RESULTS: The antisense drug inhibited growth of K562 and downregulated expression of VEGF protein significantly, compared with Scrambed control group and showed dose-dependent relation. Signs of apoptosis of K562 cells were not observed. CONCLUSION: Inhibition of K562 cell proliferation, but not cells apoptosis induction is the mechanism of inhibing growth of K562 cells by antisense drug targeted VEGF mRNA. At same time, VEGF has function of promoting K562 cell proliferation, and VEGF mRNA may be a new target attached by drugs.  相似文献   
50.
AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (105 U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC.  相似文献   
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