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371.
Loss of microbial diversity is considered a major threat because of its importance for ecosystem functions, but there is a lack of conclusive evidence that diversity itself is reduced under anthropogenic stress, and about the consequences of diversity loss. Heavy metals are one of the largest, widespread pollutant types globally, and these represent a significant environmental stressor for terrestrial microbial communities. Using combined metagenomics and functional assays, we show that the compositional and functional response of microbial communities to long‐term heavy metal stress results in a significant loss of diversity. Our results indicate that even at a moderate loss of diversity, some key specialized functions (carried out by specific groups) may be compromised. Together with previous work, our data suggest disproportionate impact of contamination on microbes that carry out specialized, but essential, ecosystem functions. Based on these findings, we propose a conceptual framework to explicitly consider diversity of functions and microbial functional groups to test the relationship between biodiversity and soil functions.  相似文献   
372.
Structure-activity relationships for a recently discovered thiazolyl phenyl ether series of acetyl-CoA carboxylase (ACC) inhibitors were investigated. Preliminary efforts to optimize the series through modification of the distal aryl ether moiety of the lead scaffold resulted in the identification of compounds exhibiting low-nanomolar potency and isozyme-selective ACC2 activity.  相似文献   
373.
Soil mono- and disaccharides (SS) and total free amino acids (AA) can influence soil microbial activities, whether they are derived from decomposition of organic materials or from plant root exudates. To quantify the relative importance of aboveground plant litter input and belowground inputs of root exudates and root debris on SS and AA, we conducted litter removal, root trenching and tree girdling experiments in a subtropical moist forest of southwest China. We found that concentrations of SS and AA had pronounced seasonal fluctuations. Litter removal markedly reduced SS concentrations, but it had no effect on AA concentrations. Concentrations of SS were significantly correlated with litterfall that had occurred 2 months earlier in the control plots, but that correlation was not observed in the litter removal plots. Multiple-linear regressions of soil respiration and soil temperature on AA concentrations were significant in both control and litter removal plots, but not in the root trenching or tree girdling plots. These results suggest that SS levels are likely to be regulated by aboveground plant litter input, and concentrations of AA are affected by microbial activity that fluctuates with soil temperature and belowground carbon input.  相似文献   
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375.
景宁玉兰是萌生能力很强的灌木树种,为了解不同生境下景宁玉兰萌枝形态及其生殖特征,选择了灌丛(SH)、黄山松林(PTF)、落叶阔叶林(DBF)、杉木林(CLF)和林缘(FE)等5种坡向一致的生境类型,通过典型样地调查,比较分析了5种不同生境下景宁玉兰萌枝数量、大小、高度、枝系、开花及结实等性状。结果表明:(1)景宁玉兰在黄山松林下的分布密度最高,但5种生境下景宁玉兰每丛的萌枝数量没有差异,每丛最大萌枝基径对每丛萌枝数有一定影响,但最大萌枝高度与每丛萌枝数没有关系。在所有调查的景宁玉兰居群中,大于2根以上萌枝的灌丛达82.5%,说明萌生更新在种群繁衍中发挥着重要作用。(2)在落叶阔叶林下的萌枝基径显著小于其他生境(P0.05),黄山松林下一级枝粗度和长度显著小于其他生境(P0.05);灌丛中的总分枝率和逐步分枝率最高,灌丛和林缘生境的逐步分枝率(SBR2:3)高于其他生境。(3)生殖萌枝基径(r=0.320,P0.05)和高度(r=0.349,P0.05)与花量均呈显著正相关关系。杉木林下景宁玉兰生殖萌枝的花量显著高于黄山松林、落叶阔叶林和林缘生境(P0.05)。虽然黄山松林下景宁玉兰萌枝开花率及开花萌枝比例最低,但其果实大小、单果种子粒数及每丛结实率却较高(P0.05),(4)景宁玉兰对环境变化极为敏感,生境类型和海拔对萌枝形态和生殖性状均有一定影响。研究表明,景宁玉兰萌生特征主要受其内在生物学特性所控制,而萌枝形态及生殖特征则与其所处环境条件更为密切。  相似文献   
376.
Elevated nitrate in the environment inhibits sulfate reduction by important microorganisms of sulfate-reducing bacteria (SRB). Several SRB may respire nitrate to survive under elevated nitrate, but how SRB that lack nitrate reductase survive to elevated nitrate remains elusive. To understand nitrate adaptation mechanisms, we evolved 12 populations of a model SRB (i.e., Desulfovibrio vulgaris Hildenborough, DvH) under elevated NaNO3 for 1000 generations, analyzed growth and acquired mutations, and linked their genotypes with phenotypes. Nitrate-evolved (EN) populations significantly (p < 0.05) increased nitrate tolerance, and whole-genome resequencing identified 119 new mutations in 44 genes of 12 EN populations, among which six functional gene groups were discovered with high mutation frequencies at the population level. We observed a high frequency of nonsense or frameshift mutations in nitrosative stress response genes (NSR: DVU2543, DVU2547, and DVU2548), nitrogen regulatory protein C family genes (NRC: DVU2394-2396, DVU2402, and DVU2405), and nitrate cluster (DVU0246-0249 and DVU0251). Mutagenesis analysis confirmed that loss-of-functions of NRC and NSR increased nitrate tolerance. Also, functional gene groups involved in fatty acid synthesis, iron regulation, and two-component system (LytR/LytS) known to be responsive to multiple stresses, had a high frequency of missense mutations. Mutations in those gene groups could increase nitrate tolerance through regulating energy metabolism, barring entry of nitrate into cells, altering cell membrane characteristics, or conferring growth advantages at the stationary phase. This study advances our understanding of nitrate tolerance mechanisms and has important implications for linking genotypes with phenotypes in DvH.Subject terms: Population genetics, Mutation  相似文献   
377.
One of the malignant transformation hallmarks is metabolism reprogramming, which plays a critical role in the biosynthetic needs of unchecked proliferation, abrogating cell death programs, and immunologic escape. However, the mechanism of the metabolic switch is not fully understood. Here, we found that the S-nitrosoproteomic profile of endogenous nitrogen oxide in ovarian cancer cells targeted multiple components in metabolism processes. Phosphofructokinase (PFKM), one of the most important regulatory enzymes of glycolysis, was S-nitrosylated by nitric oxide synthase NOS1 at Cys351. S-nitrosylation at Cys351 stabilized the tetramer of PFKM, leading to resist negative feedback of downstream metabolic intermediates. The PFKM-C351S mutation decreased the proliferation rate of cultured cancer cells, and reduced tumor growth and metastasis in the mouse xenograft model. These findings indicated that S-nitrosylation at Cys351 of PFKM by NOS1 contributes to the metabolic reprogramming of ovarian cancer cells, highlighting a critical role of endogenous nitrogen oxide on metabolism regulations in tumor progression.Subject terms: Cancer metabolism, Nitrosylation  相似文献   
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