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981.
AIM: To examine the effects of L-carnitine on apoptosis and oxidant injury in cultured neonatal rat cardiomyocytes induced by hypoxia/reoxygenation and its possible mechanism. METHODS: The cultured cardiomyocytes were divided into three groups, control, A/R group (anoxia for 120 min, reoxygenation for 240 min) and L-carnitine treatment group, in which cells were exposed to 20 mg/L, 50 mg/L, 100 mg/L, 200 mg/L L-carnitine respectively at 2 h before anoxia. The superoxide dismutase (SOD), succinate dehydrogenase (SDH) activities and malondialdehyde (MDA) content were examined, and the apoptosis was determined by flow of cytometry (FCM). In addition, the ultrastructure was observed by transmission electron microscopy. RESULTS: In A/R group, SOD and SDH activities were lower, the apoptosis rate and MDA content were higher than those in control group (P<0.05). In L-carnitine treatment group, SOD and SDH activities were higher, the apoptosis rate and MDA content were lower than those in A/R group, a L-carnitine concentration-dependent effect was found. Moreover, impairment of myocardial ultrastructure was more severe in A/R group than L-carnitine treatment group. CONCLUSION: L-carnitine can protect cardiomyocytes against hypoxia/reoxygenation-induced injury in a dose-dependent manner.  相似文献   
982.
AIM: To observe the effects of ginkgolide B on the neuron apoptosis induced by glutamate and explore whether this effects are related to the changes of calcium in neurons. METHODS: Primary neuron culture was prepared according to a previously reported procedure with slight modification. Neuron damage was induced by 0.8 mmol/L glutamate. The cell survival rate was examined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays. The neuron morphological changes, Hoechst 33258 unclear-staining analysis and agarose gel electrophoresis of DNA were measured as the indexes of cell apoptosis. Intracellular free Ca2+ concentration in neurons was measured by using the fluorescent Ca2+ indicator Fura-2/AM. RESULTS: The cells, exposed to glutamate (0.8 mmol/L), showed characteristic change of apoptosis and calcium overload, which were relieved by the treatment of ginkgolide B (10-250 μmol/L), with survival increasing and cell morphology restoring and DNA fragment decreasing. CONCLUSIONS: Ginkgolide B prevents the neurons from glutamate neurotoxicity by inhibiting glutamate-induced apoptosis. The potential mechanism of its action may be related to the competitive PAF receptor binding of ginkgolide B and decreasing the intracellular calcium concentration in neurons.  相似文献   
983.
AIM: To study the effect of extrogenous low concentration polyamine on cardiomyocyte calcium overload caused by anoxia and reoxygenation. METHODS: Enzymatically isolated rat ventricular myocytes were perfused with normal Tyrode solution for 8 min, then change to anoxia solution for 32 min, at last back to normal Tyrode solution perfusion for 8 min to establish the cardiomyocyte model of anoxia and reoxygenation. Spermine was added extracellularly to the bath before anoxia and spermine, spermidine or putrescine was added extracellularly after reoxygenation. Intracellular calcium fluorescence intensity (FI) was measured continuously by laser scan confocal microscope (LSCM). RESULTS: In the unstimulated state, exogenous spermine (1 mol/L) did not change resting [Ca2+]i in the rat cardiomyocytes. Adding spermine before anoxia antagonized the [Ca2+]i elevating caused by anoxia/reoxygenation. Adding spermine after reoxygenation also lowed the enhanced [Ca2+]i caused by reoxygenation. Considering the potency of two conditions, the former was more efficacious than the later. Spermidine and putrescine also lowed the enhanced [Ca2+]i caused by reoxygenation, but they were less efficacious than spermine. CONCLUSIONS: The results indicate that spermine given before anoxia or after reoxygenation, antagonized or lowed the cardiomyocytes calcium overload caused by anoxia/reoxygenation, but the later was weaker than the former. The order of potency of the polyamine lighten cardiomyocytes calcium overload caused by anoxia/reoxygenation was spermine>spermindine>putrescine.  相似文献   
984.
AIM: To investigate if beta2-adrenergic receptors result in more Ca2+ load after myocardial infarction (MI), the effects of beta2-adrenergic blocker on cytosolic Ca2+ ([Ca2+]i) were studied. METHODS: Male Wistar rats underwent a ligation of left coronary artery (n=9) or a sham operation (n=3). Cardiomyocytes were dissociated at 2, 4 and 8 weeks after MI and [Ca2+]i was measured via fura-2 fluorescence. The response of cardiomyocytes to isoproterenol (1 μmol/L) in the presence or absence of atenolol (1 μmol/L), beta2-adrenergic blocker ICI118,551 (0.1 μmol/L) or propranolol (1 μmol/L) was examined. RESULTS: ICI118,551 suppressed the increase in [Ca2+]i induced by isoproterenol at 4 and 8 weeks after MI (24.5%±5.7% vs 57.8%±13.2%, P<0.01; 12.2%±7.9% vs 44.6%±11.3%, P<0.01), but had no effects in control and 2 weeks post-MI groups. It decreased [Ca2+]i in control and the three post-MI groups by 14.3%, 7.9%, 57.6% and 72.6%, respectively. Atenolol had suppressive effects only in control and 2 weeks post-MI groups (P<0.05). Propranolol had suppressive effects in control and all three post-MI groups (P<0.01). CONCLUSION: Beta 2-adrenergic blocker ICI118,551 exerts negative effects on [Ca2+]i after MI, and the effects dramatically increase with the progression of MI.  相似文献   
985.
AIM: To detect the effects of NK cells on the etiology of severe pre-eclampsia. METHODS: The peripheral blood and umbilical blood from severe pre-eclamptic patients and normal late pregnant women were collected. NK cells were seperated in percoll and counted by SAP. The proliferating ability of NK cells was measured by MTT and killing power of NK cells was determined by [51Cr] releasing test. The immunohistochemistry method was used to detect the quantity of NK cells and the expression of HLA-G in placenta of them. RESULTS: (1) Compared with that in normal late pregnant women, the counts of the NK cells in peripheral blood, umbilical blood and decidua of severe pre-eclamptic patients were significantly higher (all P<0.05). (2) Compared with that in normal late pregnant women, proliferating and killing ability of NK cells in peripheral blood and umbilical blood of severe pre-eclamptic patients were significantly higher. (3) The expression of HLA-G protein in placenta of severe pre-eclampsia group was lower than that in normal group (P<0.05). CONCLUSION: The quantity of NK cells in severe pre-eclamptic patients is increased with stronger biologic function. They may be related with the pathogenesis of severe pre-eclampsia.  相似文献   
986.
茄科植物内生细菌的分离及拮抗菌的筛选   总被引:4,自引:0,他引:4  
从番茄和辣椒植株中共分离到9株对植物病原真菌具有拈抗作用的内生细菌。其中,来自樱桃番茄的内生细菌株系BS-1和湘研辣椒的内生细菌株系BS-4对辣椒根腐病菌等具有较强的拈抗作用,两者在植株体内均可以定殖。BS-1和BS-4均属于芽孢杆菌。  相似文献   
987.
杨树基因工程研究进展   总被引:1,自引:0,他引:1  
杨品前 《江西植保》2005,28(1):21-25
杨树(Populus)是世界上广泛栽培的重要造林树种之一,具有广泛的用途。近年来,杨树基因工程研究进展迅速,本文就近年来国内外学者对杨树基因工程研究成果进行了综述。  相似文献   
988.
应用CPV林间进行越冬代马尾松毛虫防治试验,结果表明不同剂量CPV与1/100000的20%氰戊菊酯乳油复配能显著提高CPV的林间杀虫效果。林间以CPV2.4×106~1.5×105多角体/ml与1/100000的20%氰戊菊酯乳油复配防治越冬代马尾松毛虫为宜,13天幼虫死亡率可达85%以上。  相似文献   
989.
AIM: To investigate the effect of recombinant human interleukin-10 (rhIL-10) on IL-6 and TNF-α levels in serum and liver of mice exposed to lipopolysaccharide (LPS). METHODS: rhIL-10 was prepared by using genetic engineering technology. Mice were intraperitoneally with 500 μg of LPS, and then were treated intravenously with various dosages of rhIL-10. The levels of IL-6 and TNF-α in hepatic tissue and serum were determined by ELISA at 12 h, 24 h, 48 h and 72 h post rhIL-10 treatment. RESULTS: rhIL-10 markedly inhibited the increase in IL-6 and TNF-α levels in hepatic tissue and serum at 12 h after rhIL-10 treatment in LPS-challenged mice, and the inhibition effect was significant at 24-48 h after rhIL-10 treatment (P<0.05). CONCLUSION: rhIL-10 can inhibit the increase in IL-6 and TNF-α levels induced by LPS in mice.  相似文献   
990.
AIM: To down-regulate expression of c-myc through antisense therapy and to investigate its effect on the sensitivity of osteosarcoma MG-63 cells to cisplatin-induced apoptosis. METHODS: The recombinant adenovirus (Ad-Asc-myc) encoding antisense c-myc fragment was constructed and transfected into osteosarcoma MG-63 cells in vitro in order to down-regulate the expression of c-myc, and the change in the sensitivity to cisplatin-induced apoptosis was observed. MTT, Western blot, RT-PCR, flow cytometry (FCM) and electron microscope were used to evaluate tumor cell proliferation in vitro, genes expression related to apoptosis regulation and effects on the sensitivity of osteosarcoma MG-63 cells to cisplatin-induced apoptosis. RESULTS: Ad-Asc-myc down-regulated the expression of c-myc protein after transfected MG-63 cells for 48 h, combined with the treatment of 2.0 mg/L cisplatin for 2 h inhibited tumor cell proliferation in vitro by 38.0%. RT-PCR revealed that Ad-Asc-myc down-regulated the expression of Bcl-2 and up-regulated the expression of Bax. No appreciable change was observed in the expression of E2F-1. FCM showed that Ad-Asc-myc induced apoptosis in intransfected cells, and rendered it more sensitive to cisplatin. CONCLUSION: Antisense c-myc is able per se to induce apoptosis and sensitize osteosarcoma cells to cisplatin-induced apoptosis.  相似文献   
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