全文获取类型
收费全文 | 1098篇 |
免费 | 89篇 |
出版年
2022年 | 9篇 |
2021年 | 12篇 |
2020年 | 11篇 |
2019年 | 8篇 |
2018年 | 8篇 |
2017年 | 10篇 |
2016年 | 23篇 |
2015年 | 48篇 |
2014年 | 53篇 |
2013年 | 61篇 |
2012年 | 66篇 |
2011年 | 69篇 |
2010年 | 36篇 |
2009年 | 55篇 |
2008年 | 79篇 |
2007年 | 52篇 |
2006年 | 61篇 |
2005年 | 66篇 |
2004年 | 70篇 |
2003年 | 70篇 |
2002年 | 66篇 |
2001年 | 12篇 |
2000年 | 14篇 |
1999年 | 12篇 |
1998年 | 17篇 |
1997年 | 13篇 |
1996年 | 11篇 |
1995年 | 14篇 |
1994年 | 9篇 |
1993年 | 9篇 |
1992年 | 10篇 |
1991年 | 10篇 |
1990年 | 10篇 |
1989年 | 6篇 |
1988年 | 9篇 |
1987年 | 5篇 |
1986年 | 3篇 |
1985年 | 4篇 |
1984年 | 8篇 |
1983年 | 5篇 |
1982年 | 9篇 |
1981年 | 8篇 |
1980年 | 3篇 |
1979年 | 8篇 |
1978年 | 5篇 |
1977年 | 4篇 |
1976年 | 5篇 |
1975年 | 5篇 |
1974年 | 8篇 |
1970年 | 3篇 |
排序方式: 共有1187条查询结果,搜索用时 31 毫秒
101.
Projecting future expansion of invasive species: comparing and improving methodologies for species distribution modeling
下载免费PDF全文
![点击此处可从《Global Change Biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Kumar P. Mainali Dan L. Warren Kunjithapatham Dhileepan Andrew McConnachie Lorraine Strathie Gul Hassan Debendra Karki Bharat B. Shrestha Camille Parmesan 《Global Change Biology》2015,21(12):4464-4480
Modeling the distributions of species, especially of invasive species in non‐native ranges, involves multiple challenges. Here, we developed some novel approaches to species distribution modeling aimed at reducing the influences of such challenges and improving the realism of projections. We estimated species–environment relationships for Parthenium hysterophorus L. (Asteraceae) with four modeling methods run with multiple scenarios of (i) sources of occurrences and geographically isolated background ranges for absences, (ii) approaches to drawing background (absence) points, and (iii) alternate sets of predictor variables. We further tested various quantitative metrics of model evaluation against biological insight. Model projections were very sensitive to the choice of training dataset. Model accuracy was much improved using a global dataset for model training, rather than restricting data input to the species’ native range. AUC score was a poor metric for model evaluation and, if used alone, was not a useful criterion for assessing model performance. Projections away from the sampled space (i.e., into areas of potential future invasion) were very different depending on the modeling methods used, raising questions about the reliability of ensemble projections. Generalized linear models gave very unrealistic projections far away from the training region. Models that efficiently fit the dominant pattern, but exclude highly local patterns in the dataset and capture interactions as they appear in data (e.g., boosted regression trees), improved generalization of the models. Biological knowledge of the species and its distribution was important in refining choices about the best set of projections. A post hoc test conducted on a new Parthenium dataset from Nepal validated excellent predictive performance of our ‘best’ model. We showed that vast stretches of currently uninvaded geographic areas on multiple continents harbor highly suitable habitats for parthenium. However, discrepancies between model predictions and parthenium invasion in Australia indicate successful management for this globally significant weed. 相似文献
102.
103.
Development of a high-density cranberry SSR linkage map for comparative genetic analysis and trait detection 总被引:2,自引:0,他引:2
Brandon Schlautman Giovanny Covarrubias-Pazaran Luis A. Diaz-Garcia Jennifer Johnson-Cicalese Massimo Iorrizo Lorraine Rodriguez-Bonilla Tierney Bougie Tiffany Bougie Eric Wiesman Shawn Steffan James Polashock Nicholi Vorsa Juan Zalapa 《Molecular breeding : new strategies in plant improvement》2015,35(8):1-18
104.
105.
106.
Review of Florida Red Tide and Human Health Effects 总被引:1,自引:0,他引:1
Fleming LE Kirkpatrick B Backer LC Walsh CJ Nierenberg K Clark J Reich A Hollenbeck J Benson J Cheng YS Naar J Pierce R Bourdelais AJ Abraham WM Kirkpatrick G Zaias J Wanner A Mendes E Shalat S Hoagland P Stephan W Bean J Watkins S Clarke T Byrne M Baden DG 《Harmful algae》2011,10(2):224-233
This paper reviews the literature describing research performed over the past decade on the known and possible exposures and human health effects associated with Florida red tides. These harmful algal blooms are caused by the dinoflagellate, Karenia brevis, and similar organisms, all of which produce a suite of natural toxins known as brevetoxins. Florida red tide research has benefited from a consistently funded, long term research program, that has allowed an interdisciplinary team of researchers to focus their attention on this specific environmental issue-one that is critically important to Gulf of Mexico and other coastal communities. This long-term interdisciplinary approach has allowed the team to engage the local community, identify measures to protect public health, take emerging technologies into the field, forge advances in natural products chemistry, and develop a valuable pharmaceutical product. The Review includes a brief discussion of the Florida red tide organisms and their toxins, and then focuses on the effects of these toxins on animals and humans, including how these effects predict what we might expect to see in exposed people. 相似文献
107.
Pitcher GM Kalia LV Ng D Goodfellow NM Yee KT Lambe EK Salter MW 《Nature medicine》2011,17(4):470-478
Hypofunction of the N-methyl D-aspartate subtype of glutamate receptor (NMDAR) is hypothesized to be a mechanism underlying cognitive dysfunction in individuals with schizophrenia. For the schizophrenia-linked genes NRG1 and ERBB4, NMDAR hypofunction is thus considered a key detrimental consequence of the excessive NRG1-ErbB4 signaling found in people with schizophrenia. However, we show here that neuregulin 1β-ErbB4 (NRG1β-ErbB4) signaling does not cause general hypofunction of NMDARs. Rather, we find that, in the hippocampus and prefrontal cortex, NRG1β-ErbB4 signaling suppresses the enhancement of synaptic NMDAR currents by the nonreceptor tyrosine kinase Src. NRG1β-ErbB4 signaling prevented induction of long-term potentiation at hippocampal Schaffer collateral-CA1 synapses and suppressed Src-dependent enhancement of NMDAR responses during theta-burst stimulation. Moreover, NRG1β-ErbB4 signaling prevented theta burst-induced phosphorylation of GluN2B by inhibiting Src kinase activity. We propose that NRG1-ErbB4 signaling participates in cognitive dysfunction in schizophrenia by aberrantly suppressing Src-mediated enhancement of synaptic NMDAR function. 相似文献
108.
Holden NJ Savage CO Young SP Wakelam MJ Harper L Williams JM 《Molecular medicine (Cambridge, Mass.)》2011,17(11-12):1242-1252
Dysregulated release of neutrophil azurophilic granules causes increased tissue damage and amplified inflammation during autoimmune disease. Antineutrophil cytoplasmic antibodies (ANCAs) are implicated in the pathogenesis of small vessel vasculitis and promote adhesion and exocytosis in neutrophils. ANCAs activate specific signal transduction pathways in neutrophils that have the potential to be modulated therapeutically to prevent neutrophil activation by ANCAs. We have investigated a role for diacylglycerol kinase (DGK) and its downstream product phosphatidic acid (PA) in ANCA-induced neutrophil exocytosis. Neutrophils incubated with the DGK inhibitor R59022, before treatment with ANCAs, exhibited a reduced capacity to release their azurophilic granules, demonstrated by a component release assay and flow cytometry. PA restored azurophilic granule release in DGK-inhibited neutrophils. Confocal microscopy revealed that R59022 did not inhibit translocation of granules, indicating a role for DGK during the process of granule fusion at the plasma membrane. In investigating possible mechanisms by which PA promotes neutrophil exocytosis, we demonstrated that exocytosis can only be restored in R59022-treated cells through simultaneous modulation of membrane fusion and increasing cytosolic calcium. PA and its associated pathways may represent viable drug targets to reduce tissue injury associated with ANCA-associated vasculitic diseases and other neutrophilic inflammatory disorders. 相似文献
109.
Dendritic spines are dynamic structures that accommodate the majority of excitatory synapses in the brain and are influenced by extracellular signals from presynaptic neurons, glial cells, and the extracellular matrix (ECM). The ECM surrounds dendritic spines and extends into the synaptic cleft, maintaining synapse integrity as well as mediating trans-synaptic communications between neurons. Several scaffolding proteins and glycans that compose the ECM form a lattice-like network, which serves as an attractive ground for various secreted glycoproteins, lectins, growth factors, and enzymes. ECM components can control dendritic spines through the interactions with their specific receptors or by influencing the functions of other synaptic proteins. In this review, we focus on ECM components and their receptors that regulate dendritic spine development and plasticity in the normal and diseased brain. 相似文献
110.
Many mechanisms purport to explain how nutritional signals during early development are manifested as disease in the adult offspring. While these describe processes leading from nutritional insult to development of the actual pathology, the initial underlying cause of the programming effect remains elusive. To establish the primary drivers of programming, this study aimed to capture embryonic gene and protein changes in the whole embryo at the time of nutritional insult rather than downstream phenotypic effects. By using a cross-over design of two well established models of maternal protein and iron restriction we aimed to identify putative common "gatekeepers" which may drive nutritional programming.Both protein and iron deficiency in utero reduced the nephron complement in adult male Wistar and Rowett Hooded Lister rats (P<0.05). This occurred in the absence of damage to the glomerular ultrastructure. Microarray, proteomic and pathway analyses identified diet-specific and strain-specific gatekeeper genes, proteins and processes which shared a common association with the regulation of the cell cycle, especially the G1/S and G2/M checkpoints, and cytoskeletal remodelling. A cell cycle-specific PCR array confirmed the down-regulation of cyclins with protein restriction and the up-regulation of apoptotic genes with iron deficiency.The timing and experimental design of this study have been carefully controlled to isolate the common molecular mechanisms which may initiate the sequelae of events involved in nutritional programming of embryonic development. We propose that despite differences in the individual genes and proteins affected in each strain and with each diet, the general response to nutrient deficiency in utero is perturbation of the cell cycle, at the level of interaction with the cytoskeleton and the mitotic checkpoints, thereby diminishing control over the integrity of DNA which is allowed to replicate. These findings offer novel insight into the primary causes and mechanisms leading to the pathologies which have been identified by previous programming studies. 相似文献