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排序方式: 共有171条查询结果,搜索用时 218 毫秒
51.
Ryan W. Speir Jonathan D. Stallings Jared M. Andrews Mary S. Gelnett Timothy C. Brand Shashikumar K. Salgar 《PloS one》2015,10(5)
Renal ischemia-reperfusion (IR) causes acute kidney injury (AKI) with high mortality and morbidity. The objective of this investigation was to ameliorate kidney IR injury and identify novel biomarkers for kidney injury and repair. Under general anesthesia, left renal ischemia was induced in Wister rats by occluding renal artery for 45 minutes, followed by reperfusion and right nephrectomy. Thirty minutes prior to ischemia, rats (n = 8/group) received Valproic Acid (150 mg/kg; VPA), Dexamethasone (3 mg/kg; Dex) or Vehicle (saline) intraperitoneally. Animals were sacrificed at 3, 24 or 120 h post-IR. Plasma creatinine (mg/dL) at 24 h was reduced (P<0.05) in VPA (2.7±1.8) and Dex (2.3±1.2) compared to Vehicle (3.8±0.5) group. At 3 h, urine albumin (mg/mL) was higher in Vehicle (1.47±0.10), VPA (0.84±0.62) and Dex (1.04±0.73) compared to naïve (uninjured/untreated control) (0.14±0.26) group. At 24 h post-IR urine lipocalin-2 (μg/mL) was higher (P<0.05) in VPA, Dex and Vehicle groups (9.61–11.36) compared to naïve group (0.67±0.29); also, kidney injury molecule-1 (KIM-1; ng/mL) was higher (P<0.05) in VPA, Dex and Vehicle groups (13.7–18.7) compared to naïve group (1.7±1.9). Histopathology demonstrated reduced (P<0.05) ischemic injury in the renal cortex in VPA (Grade 1.6±1.5) compared to Vehicle (Grade 2.9±1.1). Inflammatory cytokines IL1β and IL6 were downregulated and anti-apoptotic molecule BCL2 was upregulated in VPA group. Furthermore, kidney DNA microarray demonstrated reduced injury, stress, and apoptosis related gene expression in the VPA administered rats. VPA appears to ameliorate kidney IR injury via reduced inflammatory cytokine, apoptosis/stress related gene expression, and improved regeneration. KIM-1, lipocalin-2 and albumin appear to be promising early urine biomarkers for the diagnosis of AKI. 相似文献
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Ibeawuchi Mbanu Gregory A. Wellenius Murray A. Mittleman Lynne Peeples Leonard A. Stallings 《Chronobiology international》2013,30(4):715-726
United States firefighters have a high on‐duty fatality rate, and coronary heart disease is the leading cause. Seasonality affects the incidence of cardiovascular events in the general population, but its effects on firefighters are unknown. This study statistically examined the seasonal and annual variation of all on‐duty coronary heart disease deaths among US firefighters between 1994 and 2004 using the chi‐square distribution and Poisson regression model of the monthly fatality counts. It also examined the effect of ambient temperature (apparent as well as wind chill temperature) on coronary heart disease fatalities during the study span using a time‐stratified, case‐crossover study design. When grouped by season, we observed the distribution of the 449 coronary heart disease fatalities to show a relative peak in winter (32%) and relative nadir in spring (21%). This pattern was significantly different (p=0.005) from the expected distribution under the null hypothesis of season having no effect. The pattern persisted in additional analyses, stratifying the deaths by the type of duty in which the firefighters were engaged at the time of their deaths. In the Poisson regression model of the monthly fatality counts, the overall goodness‐of‐fit between the actual and predicted case counts was excellent (χ42=16.63; p=0.002). Two distinct peaks were detected: one in January–February and the other in August–September. Overall temperature was not associated with increased risk of on‐duty death. After allowing for different effects of temperature in mild/hot versus cold periods, a 1°C increase was not protective in cold weather; nor did it increase the risk of death in warmer weather. The findings of this study reveal statistical evidence for excess coronary heart disease deaths among firefighters during winter; however, the temporal pattern of coronary heart disease deaths was not linked to temperature variation. The seasonal pattern was also found to be independent of duty‐related risks. 相似文献
54.
James A. Nelson Christopher D. Stallings William M. Landing Jeffery Chanton 《Ecosystems》2013,16(6):1130-1138
We evaluated the potential contribution of allochthonous biomass subsidies to the upper trophic levels of offshore food webs in the northeastern Gulf of Mexico (GOM). We made this evaluation considering nitrogen, an essential and often limiting nutrient in coastal ecosystems, to estimate the potential production of within-ecosystem biomass relative to the known import of biomass from an adjacent seagrass-dominated ecosystem. When adjusted for trophic transfer efficiency, we found the biomass subsidy from a single species (pinfish, Lagodon rhomboides) from nearshore seagrass habitat to the offshore GOM to be greater than the amount of nitrogen exported by two major rivers and local submarine ground water discharge. Our calculations show that seagrass-derived biomass accounts for approximately 25% of the total potential production in the northeastern GOM. This estimate is in agreement with a previous study that found 18.5–25% of the biomass in a predatory reef fish was derived from seagrass biomass inputs. These results indicate that all of the sources we consider account for the majority of the nitrogen available to the food web in the northeastern GOM. Our approach could be adapted to other coupled ecosystems to determine the relative importance of biomass subsidies to coastal ocean food webs. 相似文献
55.
Using the twin pairs sample from the National Longitudinal Study ofAdolescent Health, we estimate bivariate Cholesky models for the influence of stressful life events (SLEs) on depressive symptoms. We show that depressive symptoms (h2Depression = .28) and dependent SLEs (events influenced by an individual's behavior) are both moderately heritable (h2SLE Dependent = .43). We find no evidence for the heritability of independent SLEs. Results from the bivariate Cholesky model suggest that roughly one-half of the correlation between depression and dependent SLEs is due to common genetic factors. Our findings suggest that attempts to characterize the causal effect of SLEs on mental health should limit their list of SLEs to those that are outside of the control of the individual. 相似文献
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57.
Mohamed Diwan M. AbdulHameed Gregory J. Tawa Kamal Kumar Danielle L. Ippolito John A. Lewis Jonathan D. Stallings Anders Wallqvist 《PloS one》2014,9(11)
Toxic liver injury causes necrosis and fibrosis, which may lead to cirrhosis and liver failure. Despite recent progress in understanding the mechanism of liver fibrosis, our knowledge of the molecular-level details of this disease is still incomplete. The elucidation of networks and pathways associated with liver fibrosis can provide insight into the underlying molecular mechanisms of the disease, as well as identify potential diagnostic or prognostic biomarkers. Towards this end, we analyzed rat gene expression data from a range of chemical exposures that produced observable periportal liver fibrosis as documented in DrugMatrix, a publicly available toxicogenomics database. We identified genes relevant to liver fibrosis using standard differential expression and co-expression analyses, and then used these genes in pathway enrichment and protein-protein interaction (PPI) network analyses. We identified a PPI network module associated with liver fibrosis that includes known liver fibrosis-relevant genes, such as tissue inhibitor of metalloproteinase-1, galectin-3, connective tissue growth factor, and lipocalin-2. We also identified several new genes, such as perilipin-3, legumain, and myocilin, which were associated with liver fibrosis. We further analyzed the expression pattern of the genes in the PPI network module across a wide range of 640 chemical exposure conditions in DrugMatrix and identified early indications of liver fibrosis for carbon tetrachloride and lipopolysaccharide exposures. Although it is well known that carbon tetrachloride and lipopolysaccharide can cause liver fibrosis, our network analysis was able to link these compounds to potential fibrotic damage before histopathological changes associated with liver fibrosis appeared. These results demonstrated that our approach is capable of identifying early-stage indicators of liver fibrosis and underscore its potential to aid in predictive toxicity, biomarker identification, and to generally identify disease-relevant pathways. 相似文献
58.
Faith Dickerson Cassie Stallings Andrea Origoni Emily Katsafanas Lucy A. B. Schweinfurth Christina L. G. Savage Robert Yolken 《PloS one》2014,9(5)
Background
Elevated levels of antibodies to Cytomegalovirus (CMV) have been associated with cognitive impairment, but the quantitative relationship between CMV antibody levels and domains of cognitive functioning in younger adults has not been established.Methods
We measured IgG class antibodies to Cytomegalovirus in 521 individuals, mean age 32.8 years. Participants were selected for the absence of psychiatric disorder and of a serious medical condition that could affect brain functioning. Cognitive functioning was measured with the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), the Wisconsin Card Sorting Test, Trail Making Test part A, and the WAIS III Letter Number Sequencing subtest. Linear regression analyses were used to measure the quantitative association between cognitive scores and Cytomegalovirus IgG antibody level. Logistic regression analyses were used to measure the odds of low cognitive scores and elevated antibody levels defined as an antibody level > = 50th, 75th, and 90th percentile of the group.Results
Higher levels of CMV antibodies were associated with lower performance on RBANS Total (coefficient −1.03, p<.0002), Delayed Memory (coefficient −0.94, p<.001), Visuospatial/Constructional (coefficient −1.77, p<5×10−7), and Letter Number Sequencing (coefficient −0.15, p<.03). There was an incremental relationship between the level of CMV antibody elevation and the odds of a low RBANS Total score. The odds of a low total cognitive score were 1.63 (95th % CI 1.01, 2.64; p<.045), 2.22 (95th % CI 1.33, 3.70; p<.002), and 2.46 (95th % CI 1.24, 4.86; p<.010) with a CMV antibody level greater than or equal to the 50th, 75th, and 90th percentile respectively.Conclusions
Higher levels of Cytomegalovirus antibodies are associated with lower levels of cognitive functioning in non-elderly adults. Methods for the prevention and treatment of CMV infection should be evaluated to determine if they result in an improvement in cognitive functioning in otherwise healthy adults. 相似文献59.
60.
Anneleen Decock Maté Ongenaert Jasmien Hoebeeck Katleen De Preter Gert Van Peer Wim Van Criekinge Ruth Ladenstein Johannes H Schulte Rosa Noguera Raymond L Stallings An Van Damme Geneviève Laureys Joëlle Vermeulen Tom Van Maerken Frank Speleman Jo Vandesompele 《Genome biology》2012,13(10):1-15
ChIP-seq is a powerful method for obtaining genome-wide maps of protein-DNA interactions and epigenetic modifications. CHANCE (CHip-seq ANalytics and Confidence Estimation) is a standalone package for ChIP-seq quality control and protocol optimization. Our user-friendly graphical software quickly estimates the strength and quality of immunoprecipitations, identifies biases, compares the user's data with ENCODE's large collection of published datasets, performs multi-sample normalization, checks against quantitative PCR-validated control regions, and produces informative graphical reports. CHANCE is available at https://github.com/songlab/chance. 相似文献