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421.
John Paul Kennedy Richard F. Preziosi Jennifer K. Rowntree Ilka C. Feller 《Molecular ecology》2020,29(4):704-719
The central‐marginal hypothesis (CMH) posits that range margins exhibit less genetic diversity and greater inter‐population genetic differentiation compared to range cores. CMH predictions are based on long‐held “abundant‐centre” assumptions of a decline in ecological conditions and abundances towards range margins. Although much empirical research has confirmed CMH, exceptions remain almost as common. We contend that mangroves provide a model system to test CMH that alleviates common confounding factors and may help clarify this lack of consensus. Here, we document changes in black mangrove (Avicennia germinans) population genetics with 12 nuclear microsatellite loci along three replicate coastlines in the United States (only two of three conform to underlying “abundant‐centre” assumptions). We then test an implicit prediction of CMH (reduced genetic diversity may constrain adaptation at range margins) by measuring functional traits of leaves associated with cold tolerance, the climatic factor that controls these mangrove distributional limits. CMH predictions were confirmed only along the coastlines that conform to “abundant‐centre” assumptions and, in contrast to theory, range margin A. germinans exhibited functional traits consistent with greater cold tolerance compared to range cores. These findings support previous accounts that CMH may not be a general rule across species and that reduced neutral genetic diversity at range margins may not be a constraint to shifts in functional trait variation along climatic gradients. 相似文献
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Klaus Fischer Jürgen Kreyling Michaël Beaulieu Ilka Beil Manuela Bog Dries Bonte Stefanie Holm Sabine Knoblauch Dustin Koch Lena Muffler Pierick Mouginot Maria Paulinich J. F. Scheepens Raijana Schiemann Jonas Schmeddes Martin Schnittler Gabriele Uhl Marieke van der Maaten-Theunissen Julia M. Weier Martin Wilmking Robert Weigel Phillip Gienapp 《Heredity》2021,126(1):23
Assessing the genetic adaptive potential of populations and species is essential for better understanding evolutionary processes. However, the expression of genetic variation may depend on environmental conditions, which may speed up or slow down evolutionary responses. Thus, the same selection pressure may lead to different responses. Against this background, we here investigate the effects of thermal stress on genetic variation, mainly under controlled laboratory conditions. We estimated additive genetic variance (VA), narrow-sense heritability (h2) and the coefficient of genetic variation (CVA) under both benign control and stressful thermal conditions. We included six species spanning a diverse range of plant and animal taxa, and a total of 25 morphological and life-history traits. Our results show that (1) thermal stress reduced fitness components, (2) the majority of traits showed significant genetic variation and that (3) thermal stress affected the expression of genetic variation (VA, h2 or CVA) in only one-third of the cases (25 of 75 analyses, mostly in one clonal species). Moreover, the effects were highly species-specific, with genetic variation increasing in 11 and decreasing in 14 cases under stress. Our results hence indicate that thermal stress does not generally affect the expression of genetic variation under laboratory conditions but, nevertheless, increases or decreases genetic variation in specific cases. Consequently, predicting the rate of genetic adaptation might not be generally complicated by environmental variation, but requires a careful case-by-case consideration.Subject terms: Evolutionary genetics, Climate-change ecology, Biodiversity 相似文献
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Maria J. Cardoso Ferreira Tânia Soares Martins Steven R. Alves Ilka Martins Rosa Jonathan Vogelgsang Niels Hansen Jens Wiltfang Odete A. B. da Cruz e Silva Rui Vitorino Ana Gabriela Henriques 《Proteomics》2023,23(15):2200515
Aging is the main risk factor for the appearance of age-related neurodegenerative diseases, including Alzheimer's disease (AD). AD is the most common form of dementia, characterized by the presence of senile plaques (SPs) and neurofibrillary tangles (NFTs), the main histopathological hallmarks in AD brains. The core of these deposits are predominantly amyloid fibrils in SPs and hyperphosphorylated Tau protein in NFTs, but other molecular components can be found associated with these pathological lesions. Herein, an extensive literature review was carried out to obtain the SPs and NFTs proteomes, followed by a bioinformatic analysis and further putative biomarker validation. For SPs, 857 proteins were recovered, and, for NFTs, 627 proteins of which 375 occur in both groups and represent the common proteome. Gene Ontology (GO) enrichment analysis permitted the identification of biological processes and the molecular functions most associated with these lesions. Analysis of the SPs and NFTs common proteins unraveled pathways and molecular targets linking both histopathological events. Further, validation of a putative phosphotarget arising from the in silico analysis was performed in serum-derived extracellular vesicles from AD patients. This bioinformatic approach contributed to the identification of putative molecular targets, valuable for AD diagnostic or therapeutic intervention. 相似文献
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