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901.
AIM: To investigate the mechanisms of transdifferentiation of renal tubular epithelial cells by the observation of serial activation of embryonic pax2 and WT1 genes in chronic renal failure model of 5/6 nephrectomized injury. METHODS: Embryo of mice, cultured renal tubule cells and chronic renal failure rat model of 5/6 nephrectomized injury were established. The expressions of paired Box gene (pax2) and Willm’s tumor gene (WT1), as well as α-smooth muscle actin (α-SMA), a phenotype of mesenchymal cells, were detected by RT-PCR and immunohistochemistry techniques. RESULTS: (1) Expressions of pax2 and WT1 mRNA began at 11.5 d and 14 d of embryo and increased gradually, and expression in trace quantity at 2 weeks after birth. Immunohistochemistry analysis revealed that WT1 only expressed in the glomerular podocytes and expressions of pax2 and WT1 in adult renal tubular cells were negative. (2) Deno-expression of pax2 and WT1 in some tubular cells appeared at week 2 and peaked at week 4 in 5/6 nephrectomized rats, both showing a same trend of expression. However, pax2 showed another peak at week 10 afterwards. (3) Re-expressions of pax2 and WT1 in TEC at 0.5 and 24 h after treated with IL-1α (10 μg/L) or AngII (10-9 mol/L) were observed respectively, followed by upregulation of α-SMA expression, and mesenchymal cells characters were shown. The effects were inhibited by Ang II receptor 2 antagonist and WT1 antibody, respectively. CONCLUSION: Adult renal tubule cells acquire re-activation of embryonic pax2 and WT1 genes and phenotypes of mesenchymes when challenge with certain injuries. Deno-expression of pax2 and WT1 genes closely relates with high concentration of bioactive facors, such as AngII and IL-1, which are involved in the mechanisms of renal tubule cells transdifferentiation. 相似文献
902.
AIM: To investigate the potential relevance of miR-21 expression level to clinicopathological characteristics and patient survival. METHODS: 113 BRCA cases with more then 5 years fallow-up data were selected. Total RNA from formalin-fixed paraffin-embedded (FFPE) tissues of 113 breast cancer (BRCA) and normal adjacent tissues (NATs) were isolated for miR-21 quantitative analysis by real-time RT-PCR. RESULTS: The miR-21 expression levels in BRCA were significantly higher than those in NATs (P<0.01) with average up-regulated level of 1.74 ± 0.48. Interestingly, high level expression of miR-21 was significantly correlated with advanced clinical stage (P<0.01), lymph node metastasis (P<0.01), and shorter survival of the patients [hazard ratio (HR)=5.476, P<0.01]. Multivariate Cox regression analysis revealed that miR-21 was one of independent prognostic impacts (HR=4.133, P<0.01) on BRCA. CONCLUSION: Over-expression of miR-21 is associated with poor prognosis of BRCA and may serve as an independent prognostic marker for BRCA. 相似文献
903.
ZHAO Ji-min LU Jing LIU Kang-dong WANG Jin-jin YANG Hong-yan HUANG You-tian DONG Zi-ming 《园艺学报》2009,25(4):744-748
AIM: To investigate the signal transduction induced DNA polymerase β expression by alternariol(AOH) in NIH3T3 cells. METHODS: The NIH3T3 cells were treated with 15 μmol/L AOH for 16 h or the cells were pretreated with an inhibitor of PKA (H89) for 1 h, and then exposed to AOH. The changes of DNA polβ expression and phospho-CREB in the cells with different treatments were determined by Western blotting and immunocytochemistry analysis. RESULTS: The expression of DNA polymerase β and phospho-CREB in NIH3T3 cells induced by AOH were significantly higher than that in control group (P<0.05). However, H89 partly blocked the AOH-induced phospho-CREB and DNA polβ expression. CONCLUSION: Alternariol up-regulates DNA polymerase β expression via the PKA-CREB pathway in NIH3T3 cells. 相似文献
904.
CAI Qing-qing LIN Tian-xin FANG Xin-lan YIN Xin-bao DONG Wen HUANG Li LIN Tong-yu 《园艺学报》2009,25(5):873-876
[ABSTRACT]AIM: To study the effect of 13-methyltetradecanoic acid (13-MTD), a saturated branched-chain fatty acid, on apoptotic induction in breast carcinoma cell line MCF-7 and its underlying mechanisms. METHODS: Breast carcinoma cell line MCF-7 and normal breast epithelial cells MaEC were treated with solvent or 13-MTD at concentration of 140 mg/L. Apoptosis was analyzed by flow cytometry. Phosphorylation of JNK, p38, FADD and Akt after treated with 13-MTD were detected by Western blotting. RESULTS: 13-MTD effectively induced apoptosis of breast carcinoma cell line MCF-7 and no influence to normal breast epithelial cells MaEC, which were confirmed by flow cytometry analysis, was observed. The results of Western blotting showed that obvious increase in p38 and JNK phosphorylation. No significant difference of FADD phosphorylation was observed. However, evidently decrease in Akt phosphorylation was found after treated with 13-MTD. CONCLUSION: 13-MTD was a new safe, effective chemotherapeutic drug. Its underlying mechanisms are through activating MAPK pathway and inhibiting Akt pathway to induce the cancer cells apoptosis. 相似文献
905.
AIM: To observe the damage induced in the primary cultured rat cortical neurons by oxygen/glucose deprivation and reintroduction, and to investigate the neuroprotective mechanism of salvianolic acid B (SalB). METHODS: Primary cultured rat cortical neurons were randomly divided into the control group, the model group and the SalB group. The cell model was established by oxygen/glucose deprivation for 3 h followed oxygen/glucose reintroduction for 24 h. The cortical neurons viability was determined by MTT assay. The leakage rate of lactate dehydrogenase (LDH) was measured by chromatometry. The mitochondrial membrane potentials (MMP) and the apoptosis rate were quantitatively analyzed by flow cytometry. The cytosolic free calcium was assessed using LSCM. The morphologic changes of neuronal nuclei were observed by Hoechst 33342 fluorescence staining. RESULTS: Compared to the model group, the cortical neurons viability, the survival rate and the fluorescence value of MMP in the SalB group were obviously increased (P<0.05,P<0.01). In addition, in the SalB group, the leakage rate of LDH, the fluorescence intensity of cytosolic free calcium and the apoptosis rate were significantly lower than those in the model group (P<0.01). CONCLUSION: The neuroprotective mechanism of SalB in the oxygen/glucose deprivation and reintroduction neurons would be due to the fact that SalB maintains the MMP and the calcium homeostasis. 相似文献
906.
907.
WU Xiao-jing HUANG Lan ZHOU Qi CHEN Jian-fei ZHOU Yin-pin NIU Qin ZOU Yun-zeng GE Jun-bo 《园艺学报》2009,25(10):1873-1877
AIM: To investigate the effect of Jagged1 expression in endothelial cells (EC) on platelet derived growth factor (PDGF) induced proliferation and migration of vascular smooth muscle cells (VSMC) in rat.METHODS: Rat aorta EC was inoculated in the lower chamber and VSMC were in the upper chamber of the cell coculture system. Three groups were divided: control, sicontrol and siJagged1. The EC Jagged1 protein expression was assayed by Western blotting to evaluate small RNA interfering (RNAi) efficiency. After the cells were cocultured with PDGF for 24 h, the proliferation and migration of VSMC were respectively evaluated by [3H]-TdR incorporation and migrating cells counting. Protein expression of α-SM-actin in VSMC was assayed by Western blotting. RESULTS: The Jagged1 protein expression in EC was significantly lower in siJagged1 group than that in control group (0.26±0.02 vs 0.67±0.02, P<0.05), and no statistic significance was observed between control and sicontrol groups. The VSMC [3H]-TdR incorporation and migration were higher in PDGF +siJagged1 group than those in PDGF group {[3H]-TdR incorporation (23 074±2 702) counts·min-1·well-1 vs (16 442±1 803)counts·min-1·well-1, n=5, P<0.05; migration (27±4) cells/field vs (15±3)cells/field, n=5, P<0.05}. The α-SM-actin protein in VSMC was lower in PDGF + siJagged1 group than that in PDGF group (0.25±0.06 vs 0.49±0.04, n=3, P<0.05).CONCLUSION: Jagged1 knock down in rat EC accelerates PDGF induced proliferation and migration of VSMC. These results suggest that Jagged1 expression in EC plays an important role in maintaining VSMC contract phenotype and inhibiting VSMC overgrowth after arterial injury. 相似文献
908.
TAN Wei-ping XIA Yan WU Bao-jing LI Jing HUANG Hua-rong HUANG Shao-liang MAI Xian-di 《园艺学报》2009,25(12):2399-2402
AIM: To investigate the effect of T-bet plasmid gene transfer to airway on allergen induced airway inflammation in a murine asthmatic model. METHODS: A mouse asthma model was established by sensitization with ovalbumin (OVA). Forty C57BL/6 mice were divided into 4 groups (10 mice in each group): the normal control group (group A), the asthmatic model group (group B), the pcDNA3 plasmid group (group C), and the pcDNA3-T-bet group (group D). The animals in group B, C and D were sensitized and challenged with OVA. The animals in group A were applied with normal saline. pcDNA3 plasmid at dose of 50 μg was intranasally administered at 24 h before intranasal challenges to the mice in group C, and the 50 μg pcDNA3-T-bet plasmid for the mice in group D. Bronchial alveolar lavage fluid (BALF) was collected and lung tissues were resected at 48 h after OVA challenge for later assay. RESULTS: After administration with pcDNA3-T-bet plasmid, high level of T-bet expression at 48 h was detected in the lung tissue by Western blotting. In pcDNA3-T-bet treated asthmatic models, histological evaluation revealed the significant suppression of eosinophil peribronchial and perivascular infiltration, and reduction of epithelial damage. The numbers of eosinophils, neutrophils and lymphocytes in BALF from pcDNA3-T-bet treated mice were significantly reduced compared to those in asthmatic control group (P<0.05). The level of IL-4 in BALF was significantly decreased in pcDNA3-T-bet group compared to that in asthmatic control group (P<0.05), while the level of IFN-γ in BALF was significantly increased in pcDNA3-T-bet group. No significant change of inflammation cells and cytokines in pcDNA3 plasmid group and asthmatic control group was observed (P>0.05). CONCLUSION: Intranasal pcDNA3-T-bet plasmid transfer inhibits asthmatic airway inflammation in the murine asthmatic model, suggesting a new therapeutic strategy for allergic asthma. 相似文献
909.
WEI Chun-ying WANG Meng-hong WEI Yun-feng ZHENG Ze-qi PENG Jing-tian HUANG Jun WEN Yuan WU Zhi-yong 《园艺学报》2009,25(11):2122-2125
AIM: To investigate the effect and the mechanism of apolipoprotein (a) [apo (a)] on proliferation of vascular smooth muscle cells (VSMCs). METHODS: All VSMCs used in experiments were serial subcultured from primary cells and were identified by immunohistochemistry staining of α-actin. Cell growth assay was observed as cell counting and MTT assay. Western blotting was also employed to detect the related mechanism. RESULTS: All cells used in experiments were confirmed as VSMCs. Although apo (a) enhanced VSMCs proliferation, this effect was attenuated by anti-integrin αⅤβ3, LM609. Use these reagents alone had no effect on VSMCs growth. The results of Western blotting demonstrated that focal adhesion kinase (FAK) was activated by apo (a) and the expression of total or phosphorylated transforming growth factor β1 (TGF-β1) was also decreased. However, these effects described above were all blocked by LM609. CONCLUSION: Apolipoprotein (a) enhances VSMCs proliferation and this effect is mediated by integrin αⅤβ3, which activates FAK and attenuates TGF-β1 and phospho-TGF-β1 expression. 相似文献
910.