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Lead and di-2-ethylhexyl phthalate (DEHP) are widely distributed in the environment, and their neurotoxicity has caused a widespread concern. The complexity of environmental exposure provides the possibility of their combined exposure. The present study aims to describe a joint neurotoxicity and clarify the potential mechanism after combined exposure to lead and DEHP. A 2 × 3 factorial design was used to analyze either single effects or their interaction by a subchronic lead and DEHP exposure model of the male weaning rats. Similar to the previous study, lead or DEHP single exposure showed an increased neurotoxicity. Interestingly, our neurobehavioral test showed the rats in the combined exposure groups had a better ability of learning and memory compared with the single-exposure ones. It seemed to reflect an antagonism joint action in neurotoxicity after combined exposure. The content of dehydroepiandrosterone (DHEA) in serum and the mRNA level of brain-derived neurotrophic factor (Bdnf) in the hippocampus showed a similar trend to the ability of learning and memory. However, there was insufficient evidence to support the joint action on some indexes of oxidative stress such as malondialdehyde (MDA), the ratio of reduced glutathione(GSH) to oxidized glutathione(GSSG), γglutamylcysteine synthetase (γ-GCS), glutathione-s transferase (GST), and nuclear factor E2-related factor 2 (Nrf2) mRNA expression in the hippocampus. In a word, our current study reminded a unique antagonism joint action of neurotoxicity after combined exposure to lead and DEHP, which may contribute to understanding some shallow mechanism of the joint toxicity due to the complexity of environmental pollutant exposure.
相似文献Overexpression of cotton cellulose synthase like D3 (GhCSLD3) gene partially rescued growth defect of atcesa6 mutant with restored cell elongation and cell wall integrity mainly by enhancing primary cellulose production.
AbstractAmong cellulose synthase like (CSL) family proteins, CSLDs share the highest sequence similarity to cellulose synthase (CESA) proteins. Although CSLD proteins have been implicated to participate in the synthesis of carbohydrate-based polymers (cellulose, pectins and hemicelluloses), and therefore plant cell wall formation, the exact biochemical function of CSLD proteins remains controversial and the function of the remaining CSLD genes in other species have not been determined. In this study, we attempted to illustrate the function of CSLD proteins by overexpressing Arabidopsis AtCSLD2, -3, -5 and cotton GhCSLD3 genes in the atcesa6 mutant, which has a background that is defective for primary cell wall cellulose synthesis in Arabidopsis. We found that GhCSLD3 overexpression partially rescued the growth defect of the atcesa6 mutant during early vegetative growth. Despite the atceas6 mutant having significantly reduced cellulose contents, the defected cell walls and lower dry mass, GhCSLD3 overexpression largely restored cell wall integrity (CWI) and improved the biomass yield. Our result suggests that overexpression of the GhCSLD protein enhances primary cell wall synthesis and compensates for the loss of CESAs, which is required for cellulose production, therefore rescuing defects in cell elongation and CWI.
相似文献Amyloid-β (Aβ) plays an important role in Alzheimer’s disease (AD) pathogenesis, and growing evidence has shown that poor sleep quality is one of the risk factors for AD, but the mechanisms of sleep deprivation leading to AD have still not been fully demonstrated. In the present study, we used wild-type (WT) rats to determine the effects of chronic sleep restriction (CSR) on Aβ accumulation. We found that CSR-21d rats had learning and memory functional decline in the Morris water maze (MWM) test. Meanwhile, Aβ42 deposition in the hippocampus and the prefrontal cortex was high after a 21-day sleep restriction. Moreover, compared with the control rats, CSR rats had increased expression of β-site APP-cleaving enzyme 1 (BACE1) and sAPPβ and decreased sAPPα levels in both the hippocampus and the prefrontal cortex, and the BACE1 level was positively correlated with the Aβ42 level. Additionally, in CSR-21d rats, low-density lipoprotein receptor-related protein 1 (LRP-1) levels were low, while receptor of advanced glycation end products (RAGE) levels were high in the hippocampus and the prefrontal cortex, and these transporters were significantly correlated with Aβ42 levels. In addition, CSR-21d rats had decreased plasma Aβ42 levels and soluble LRP1 (sLRP1) levels compared with the control rats. Altogether, this study demonstrated that 21 days of CSR could lead to brain Aβ accumulation in WT rats. The underlying mechanisms may be related to increased Aβ production via upregulation of the BACE1 pathway and disrupted Aβ clearance affecting brain and peripheral Aβ transport.
相似文献Communicated by Ramaswamy H. Sarma 相似文献