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61.
CAI Yun-feng MIN Jun FANG Tian-ling CHU Zhong-hua DENG Xiao-geng HE Jing-song CHEN Ji-sheng 《园艺学报》2003,19(8):1029-1033
AIM: To explore the feasibility of direct separat and selective enlargement of the bone marrow-derived liver stem cells (BDLSC) from bone marrow cells with a culture system containing cholestatic serum in vitro. METHODS: Bone marrow cells of rats were cultured with selective media containing 2%, 5%, 7% and 10% cholestatic rat serum, respectively. The BDLSC were then induced to proliferate with the addition of hepatocyte growth factor (HGF) on the firth day. BDLSC were characterized using immunocytochemistry and RT-PCR for lineage markers, glycogen staining and urea synthetic assay for functions 2 weeks later. RESULTS: Bone marrow cells were unble to form colony in the presence of 2% cholestatic serum and apopotosis appeared gradually in 7% or 10% cholestatic serum. The BDLSC survived in the medium containing 5% cholestatic serum while the other types of cells did not. The survival cells proliferated with a high speed during the second week and then formed hepatocyte-like colony-forming units (H-CFU). Cells in the H-CFU expressed the characteristic proteins of fetal hepatocytes. Furthermore, they had glycogen storage and urea synthesis functions, two of the critical features of hepatocytes. CONCLUSION: The selective micro-environment effectively selected BDLSC from the bone marrow cell, and will be a new way to provide an abundant source of donor hepatocytes for clinical cell therapy. 相似文献
62.
AIM:The β-catenin is a key molecule in the Wnt signal pathway, which plays a critical role in normal development and tumorigenesis. However, the mechanisms of the β-catenin on the cell growth control are still not completely defined. The aim of this study was to test the hypothesis that the mutant β-catenin may regulate the hepatocyte proliferation. METHODS: The immortalized murine hepatocyte cell line, AML12, was used for this study. A plasmid that contain mutant β-catenin S33Y was transfected into the AML12 cells and a stable cell line AML12S33Y was established. The cell growth property of this cell line and the parental cell were compared by flow cytometry analysis and direct cell count. The cells were also tested for the ability to form soft agar colonies, and the ability to form tumors in the severe immune deficient mice (SCID). RESULTS:1. The mutant β-catenin containing cell line AML12S33Y has higher proliferating index compared with the parental AML12 cells (P<0.01), suggesting that mutant β-catenin promotes cell growth. 2. The mutant β-catenin cells formed small colonies in soft agar after 4 weeks of culture, but did not generate tumor in SCID mice. CONCLUSION:The mutant β-catenin promotes liver cell growth. 相似文献
63.
AIM:To study influence of ischemia-reperfusion(IR) on apoptosis and expression of apoptosis-related genes Fas-L, Bax and Bcl-2 of sinoatrial node(SAN) cells in rabbits in vivo. METHODS:Ninety healthy adult rabbits were divided randomly into control group, ischemia groups (I10 min, I30 min, I60 min and I120 min) and IR groups (I10 minR4h, I30 minR4h, I60 minR4hand I120 minR4h). IR injury model of SAN was established by occluding and loosening the start section of right coronary artery. The apoptosis of SAN cells was detected by TUNEL staining. The expression of Fas-L, Bax and Bcl-2 of SAN cells was detected by immunohistochemistry. RESULTS:①No obvious apoptosis of SAN cells was observed in control group, I10 min and I30 min groups. Apoptosis of different degrees in SAN cells were found in 68.3%(41/60) rabbits in I60 min, I120 min and 4 subgroups of IR. ②The highest expression of Fas-L and Bax was observed in I120 min group and that of Bcl-2 was in I60 min group. ③The highest expression of Fas-L and Bax was observed in I60 minR4h group. The peak level of Bcl-2 was observed in I30 minR4h group. ④The expression of Fas-L and Bax was significant higher in IR group than that in ischemic group at the same time point. CONCLUSION:Ischemia and IR induced apoptosis of SAN cells in rabbit in vivo. Fas-L、Bax、Bcl-2 may participate in the regulation of apoptosis and the injury during IR aggravates the apoptosis of SAN cells. 相似文献
64.
区域旅游资源开发定位研究——以内蒙古赤峰市为例 总被引:7,自引:1,他引:7
区域旅游资源开发是发展区域旅游的基础 ,开发的定位研究有助于为一地旅游业的发展指明方向。本文从区域角度和空间经济一体化思想出发 ,以赤峰市为例 ,通过对旅游资源的定量与定性研究 ,得到旅游资源的综合评价图式 ,结合区际分析归纳出赤峰市旅游资源开发利用的方向和层次。从而为区域旅游开发的定位研究进行了一般理论的探讨及例证分析 相似文献
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AIM:To investigate the effect of metallothionein(MT) on proliferation of rat vascular smooth muscle cells (VSMCs) stimulated by homocysteine and its mechanism. METHODS:VSMCs proliferation was measured by [3-H]-TdR incorporation, mitogen-activated protein kinase(MAPK)activity were determined by immunoprecipitation method, the intracellular contents of MT and malondialdehyde (MDA)were assayed by -hemoglobin saturation method and TBA reaction, respectively, and lactate dehydrogenase (LDH) leakage was measured by NADH oxidation. RESULTS:Hcy(10-6-10-4 mmol/L) stimulated [3-H]-TdR incorporation by the VSMCs in a concentration-dependent manner. Compared with control, [3-H]-TdR incorporation in VSMCs treated with 0.1 mmol/L Hcy was increased by 4.2 fold (P<0.01). Meanwhile, Hcy enhanced MAPK activity, MDA formation and LDH release (P<0.01)in a concentration-dependent manner. Treatment of VSMCs with MT alone did not change above parameters, compared with control. However, MT (10-6-10-4 mol/L)attenuated significantly Hcy-stimulated proliferation of VSMCs (P<0.01)in a concentration-dependent manner. And MT inhibited obviously Hcy-induced activation of MAPK activity, MDA formation and LDH release. Preincubation of VSMCs with 0.5 mmol/L ZnCl2 for 6 h induced an increase cellular MT content by 5.7-fold (P<0.01). The MT-overexpressed VSMCs resisted Hcy-stimulating action on MAPK activity, MDA formation and LDH leakage (P<0.01). CONCLUSION:These results show that MT has an inhibitory effect on Hcy-induced VSMCs proliferation, and that MT could inhibit Hcy-stimulated MAPK activity and lipid peroxidation. 相似文献
70.
AIM:To explore the expressive profile of nestin protein in the focal ischemic brain and to study the recovery mechanism of brain focal infarct.METHODS:Cellular morphology,time-course and distribution pattern of nestin positive response were immunohistochemically examined in different brain regions of 36 adult male SD rats. RESULTS:Nestin positive response of different brain regions in sham operated rats was present in small- and micro-vasculartures and the third ventricle bottom and ependyma. A large number of nestin positive cells were detected in ischemic brain, and were more remarkable in the cortical areas of parietal lobe and preoptic area as well as ischemic caudoputamen. Stellate nestin positive cells were located in the deep layer of ischemic cortex, but fibrillary cells were located in the shallow layer. Nestin positive cells in the ischemic caudoputamen showed the same changes of morphology as those cells in the deep layer of ischemic cortex. Morphological and number alterations of nestin positive cells were the most remarkable at 1 weeks post-ischemia, which showed more hypertrophy and proliferation in morphology, and a marked increase in number was present in the ischemic cerebral cortex and the ischemic caudoputamen. These alterations of nestin positive cells persisted up to 6 weeks post-ischemia, and then, the nestin positive response in the ischemic brain decreased gradually.CONCLUSION:Focal cerebral ischemia induces nestin re-expression on reactive astrocytes, which may be very important to the self-recovery of cerebral infarct. 相似文献