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31.
Jing-Jing Yang Hui Tao Cheng Huang Kai-hu Shi Tao-Tao Ma Er-Bao Bian Lei Zhang Li-Ping Liu Wei Hu Xiong-Wen Lv Jun Li 《Cellular signalling》2013,25(5):1202-1211
Hepatic stellate cell (HSC) activation plays an important role in liver fibrogenesis. Transdifferentiation of quiescent hepatic stellate cells into myofibroblastic-HSCs is a key event in liver fibrosis. The methyl-CpG-binding protein MeCP2 which promotes repressed chromatin structure is selectively detected in myofibroblasts of diseased liver. MeCP2 binds to methylated CpG dinucleotides, which are abundant in the promoters of many genes. Treatment of HSCs with DNA methylation inhibitor 5-aza-2′- deoxycytidine (5-azadC) prevented proliferation and activation. Treatment with 5-azadC prevented loss of Patched (PTCH1) expression that occurred during HSCs activation. In a search for underlying molecular medchanisms, we investigated whether the targeting of epigenetic silencing mechanisms could be useful in the treatment of PTCH1-associated fibrogenesis. It was indicated that hypermethylation of PTCH1 is associated with the perpetuation of fibroblast activation and fibrosis in the liver. siRNA knockdown of MeCP2 increased the expressions of PTCH1 mRNA and protein in hepatic myofibroblasts. These data suggest that DNA methylation and MeCP2 may provide molecular mechanisms for silencing of PTCH1. 相似文献
32.
Biochar’s effect on crop productivity and the dependence on experimental conditions—a meta-analysis of literature data 总被引:19,自引:0,他引:19
Xiaoyu Liu Afeng Zhang Chunying Ji Stephen Joseph Rongjun Bian Lianqing Li Genxing Pan Jorge Paz-Ferreiro 《Plant and Soil》2013,373(1-2):583-594
Background and aims
For the last decade, there has been an increasing global interest in using biochar to mitigate climate change by storing carbon in soil. However, there is a lack of detailed knowledge on the impact of biochar on the crop productivity in different agricultural systems. The objective of this study was to quantify the effect of biochar soil amendment (BSA) on crop productivity and to analyze the dependence of responses on experimental conditions.Methods
A weighted meta-analysis was conducted based on data from 103 studies published up to April, 2013. The effect of BSA on crop productivity was quantified by characterizing experimental conditions.Results
In the published experiments, with biochar amendment rates generally <30 t ha?1, BSA increased crop productivity by 11.0 % on average, while the responses varied with experimental conditions. Greater responses were found in pot experiments than in field, in acid than in neutral soils, in sandy textured than in loam and silt soils. Crop response in field experiments was greater for dry land crops (10.6 % on average) than for paddy rice (5.6 % on average). This result, associated with the higher response in acid and sandy textured soils, suggests both a liming and an aggregating/moistening effect of BSA.Conclusions
The analysis suggests a promising role for BSA in improving crop productivity especially for dry land crops, and in acid, poor-structured soils though there was wide variation with soil, crop and biochar properties. Long-term field studies are needed to elucidate the persistence of BSA’s effect and the mechanisms for improving crop production in a wide range of agricultural conditions. At current prices and C-trading schemes, however, BSA would not be cost-effective unless persistent soil improvement and crop response can be demonstrated. 相似文献33.
Yi-Quan Tang Ping Liang Jingheng Zhou Yanxin Lu Lei Lei Xiling Bian KeWei Wang 《The Journal of biological chemistry》2013,288(21):14727-14741
In the brain and heart, auxiliary Kv channel-interacting proteins (KChIPs) co-assemble with pore-forming Kv4 α-subunits to form a native K+ channel complex and regulate the expression and gating properties of Kv4 currents. Among the KChIP1–4 members, KChIP4a exhibits a unique N terminus that is known to suppress Kv4 function, but the underlying mechanism of Kv4 inhibition remains unknown. Using a combination of confocal imaging, surface biotinylation, and electrophysiological recordings, we identified a novel endoplasmic reticulum (ER) retention motif, consisting of six hydrophobic and aliphatic residues, 12–17 (LIVIVL), within the KChIP4a N-terminal KID, that functions to reduce surface expression of Kv4-KChIP complexes. This ER retention capacity is transferable and depends on its flanking location. In addition, adjacent to the ER retention motif, the residues 19–21 (VKL motif) directly promote closed-state inactivation of Kv4.3, thus leading to an inhibition of channel current. Taken together, our findings demonstrate that KChIP4a suppresses A-type Kv4 current via ER retention and enhancement of Kv4 closed-state inactivation. 相似文献
34.
Zheng Ma Yalin Bian Xuping Shentu Xiaoping Yu 《Applied microbiology and biotechnology》2013,97(9):4055-4064
1,3-propanediol (1,3-PDO) is one of the most important industrial chemicals due to its highly desired properties and its wide applications as a key component of the emerging polymer industry. Biotechnology route has been one of the most interesting methods for 1,3-PDO production, whereas, the dha genes were essential to 1,3-PDO biosynthesis. In this study, we cloned and placed the dha cassettes under the control of a glyceraldehyde 3-phosphate dehydrogenase gene promoter pGAP and homologous ZrFPS1 gene promoter pZrfps1; these two promoters were further integrated into the chromosome of Z. rouxii JL2011 to generate recombinant strain JL2011-GZ and JL2011-ZZ, respectively. The results showed that the two strains could produce 1,3-PDO from glucose with a final yield of 6.9 and 10.3 g/l, respectively. The engineered strain JL2011-ZZ showed a 2.3- and 1.5-fold increase in the specific activities and final concentration of 1,3-PDO, respectively, with respect to JL2011-GZ. Batch fermentation with aerobic/micro-aerobic combined strategy of JL2011-ZZ resulted a titer of 17.1 g/l and a yield from glucose of 8.6 %. These results demonstrated that JL2011-ZZ would be a potential strain for 1,3-PDO production from glucose. 相似文献
35.
d-Galactose is widely used as an agent to cause aging effects in experimental animals. The present study aims to investigate the effects of hydrogen sulfide (H2S) in human neuroblastoma SH-SY5Y cells exposed to d-galactose. Cells were pretreated with NaHS, an H2S donor, and then exposed to d-galactose (25–400 mM for 48 h). We found that NaHS pretreatment significantly reversed the d-galactose-induced cell death and cellular senescence. MTT assay shows that NaHS significantly increased cell viability from 62.31 ± 1.29% to 72.34 ± 0.46% compared with d-galactose (200 mM) treatment group. The underlying mechanism appeared to involve a reduction by NaHS in the formation of advanced glycation end products (AGEs), which are known to contribute to the progression of age-related diseases. In addition, NaHS decreased the elevation of reactive oxygen species from 151.17 ± 2.07% to 124.8 ± 2.89% and malondialdehyde from 1.72 ± 0.07 to 1.10 ± 0.08 (nmol/mg protein) in SH-SY5Y cells after d-galactose exposure. NaHS also stimulated activities of superoxide dismutase from 0.42 ± 0.05 to 0.73 ± 0.04 (U/mg protein) and glutathione peroxidase from 3.98 ± 0.73 to 14.73 ± 0.77 (nmol/min/mg protein) and upregulated the gene expression levels of copper transport protein ATOX1, glutathione synthetase (GSS) and thioredoxin reductase 1 (TXNRD1) while down-regulated aldehyde oxidase 1 (AOX1). In summary, our data indicate that H2S may have potentially anti-aging effects through the inhibition of AGEs formation and reduction of oxidative stress. 相似文献
36.
Can-Jie Guo Qin Pan Hua Xiong Yu-Qi Qiao Zhao-Lian Bian Wei Zhong Li Sheng Hai Li Lei Shen Jing Hua Xiong Ma Jing-Yuan Fang 《FEBS letters》2013
In our previous study, miR-126 was identified as one of the leading miRNAs that is downregulated during activation of hepatic stellate cells (HSCs). However, the roles and related mechanisms of miR-126 in HSCs are not understood. In this study, we compared expression of miR-126 during HSC activation both in vitro and in vivo. We also applied RNA interference to analyze the role and mechanism of miR-126∗ in the activation of HSCs. Restoring HSCs with Lv-miR-126∗ resulted in decreased proliferation, accumulation of extracellular matrix components, and cell contraction, while also negatively regulating the vascular endothelial growth factor (VEGF) signal transduction pathways by partially targeted VEGF-A. Thus, we postulate that miR-126 may be a biological marker for the activation of HSCs, and useful for reducing intrahepatic vascular resistance and improving the sinusoidal microcirculation in chronic liver diseases. 相似文献
37.
Ke Xing Guang-Kai Bian Sheng Qin Hans-Peter Klenk Bo Yuan Yue-Ji Zhang Wen-Jun Li Ji-Hong Jiang 《Antonie van Leeuwenhoek》2013,104(6):1245-1245
38.
Y Liu H Cheng Y Zhou Y Zhu R Bian Y Chen C Li Q Ma Q Zheng Y Zhang H Jin X Wang Q Chen D Zhu 《Cell death & disease》2013,4(2):e494
Myostatin, a member of the transforming growth factor-β superfamily, regulates the glucose metabolism of muscle cells, while dysregulated myostatin activity is associated with a number of metabolic disorders, including muscle cachexia, obesity and type II diabetes. We observed that myostatin induced significant mitochondrial metabolic alterations and prolonged exposure of myostatin induced mitochondria-dependent apoptosis in cancer cells addicted to glycolysis. To address the underlying mechanism, we found that the protein levels of Hexokinase II (HKII) and voltage-dependent anion channel 1 (VDAC1), two key regulators of glucose metabolisms as well as metabolic stress-induced apoptosis, were negatively correlated. In particular, VDAC1 was dramatically upregulated in cells that are sensitive to myostatin treatment whereas HKII was downregulated and dissociated from mitochondria. Myostatin promoted the translocation of Bax from cytosol to mitochondria, and knockdown of VDAC1 inhibited myostatin-induced Bax translocation and apoptosis. These apoptotic changes can be partially rescued by repletion of ATP, or by ectopic expression of HKII, suggesting that perturbation of mitochondrial metabolism is causally linked with subsequent apoptosis. Our findings reveal novel function of myostatin in regulating mitochondrial metabolism and apoptosis in cancer cells. 相似文献
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