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991.
The aim of the present investigation was to find out the effects of roscovitine treatment of donor cells and different activation methods on development of HMC goat embryos. Goat fetal fibroblast cells were cultured and divided into three treatment groups—contact inhibition group, roscovitine treatment group and serum starvation group. There was a significant decrease in blastocyst yield in serum starvation group (6.82%) compared to roscovitine treatment group (19.31%) and contact inhibition group (18.52%), however, no significant difference was found between roscovitine treatment group and contact inhibition group. To see the effect of different methods of activation, the reconstructed embryos were randomly divided into two groups and activated by two methods—one half by 2 μM Ca ionophore and another half by 2.31 kV/cm for 15 μSec electrical pulse. Subsequently, cloned embryos were cultured in TCM-199 based embryo development medium supplemented with 10 mg/mL bovine serum albumin in WOW culture system. There was a significant increase in the rate of cleavage and blastocyst production in electric pulse activation of 78.57% and 21.43% than Ca ionophore activation of 62.63% and 10.61% respectively. In conclusion, treatment of donor cells with roscovitine yields a significantly increased blastocyst than serum starved donor cells but equivalent blastocyst to contact inhibition group and electrical pulse activation (EPA) improves the production of HMC goat embryos. 相似文献
992.
993.
Kim DW Kim DS Kim MJ Kwon SW Ahn EH Jeong HJ Sohn EJ Dutta S Lim SS Cho SW Lee KS Park J Eum WS Hwang HS Choi SY 《BMB reports》2011,44(10):647-652
The protein transduction domains have been reported to have potential to deliver the exogenous molecules, including proteins, to living cells. However, poor transduction of proteins limits therapeutic application. In this study, we examined whether imipramine could stimulate the transduction efficiency of PEP-1 fused proteins into astrocytes. PEP-1-catalase (PEP-1- CAT) was transduced into astrocytes in a time- and dose-dependent manner, reducing cellular toxicity induced by H(2)O(2). Additionally, the group of PEP-1-CAT (+) imipramine showed enhancement of transduction efficiency and therefore increased cellular viability than that of PEP-1-CAT alone. In the gerbil ischemia models, PEP-1-CAT displayed significant neuroprotection in the CA1 region of the hippocampus. Interestingly, PEP-1-CAT (+) imipramine prevented neuronal cell death and lipid peroxidation more markedly than PEP-1-CAT alone. Therefore, our results suggest that imipramine can be used as a drug to enhance the transduction of PEP-1 fusion proteins to cells or animals and their efficacies against various disorders. 相似文献
994.
995.
Emergence of a globally dominant IncHI1 plasmid type associated with multiple drug resistant typhoid
Holt KE Phan MD Baker S Duy PT Nga TV Nair S Turner AK Walsh C Fanning S Farrell-Ward S Dutta S Kariuki S Weill FX Parkhill J Dougan G Wain J 《PLoS neglected tropical diseases》2011,5(7):e1245
Typhoid fever, caused by Salmonella enterica serovar Typhi (S. Typhi), remains a serious global health concern. Since their emergence in the mid-1970s multi-drug resistant (MDR) S. Typhi now dominate drug sensitive equivalents in many regions. MDR in S. Typhi is almost exclusively conferred by self-transmissible IncHI1 plasmids carrying a suite of antimicrobial resistance genes. We identified over 300 single nucleotide polymorphisms (SNPs) within conserved regions of the IncHI1 plasmid, and genotyped both plasmid and chromosomal SNPs in over 450 S. Typhi dating back to 1958. Prior to 1995, a variety of IncHI1 plasmid types were detected in distinct S. Typhi haplotypes. Highly similar plasmids were detected in co-circulating S. Typhi haplotypes, indicative of plasmid transfer. In contrast, from 1995 onwards, 98% of MDR S. Typhi were plasmid sequence type 6 (PST6) and S. Typhi haplotype H58, indicating recent global spread of a dominant MDR clone. To investigate whether PST6 conferred a selective advantage compared to other IncHI1 plasmids, we used a phenotyping array to compare the impact of IncHI1 PST6 and PST1 plasmids in a common S. Typhi host. The PST6 plasmid conferred the ability to grow in high salt medium (4.7% NaCl), which we demonstrate is due to the presence in PST6 of the Tn6062 transposon encoding BetU. 相似文献
996.
Background
Neuroinflammation associated with Japanese encephalitis (JE) is mainly due to the activation of glial cells with subsequent release of proinflammatory mediators from them. The recognition of viral RNA, in part, by the pattern recognition receptor retinoic acid-inducible gene I (RIG-I) has been indicated to have a role in such processes. Even though neurons are also known to express this receptor, its role after JE virus (JEV) infections is yet to be elucidated.Methodology/Principal Findings
Upon infecting murine neuroblastoma cells and primary cortical neurons with JEV the expression profile of key proinflammatory cyto/chemokines were analyzed by qRT-PCR and bead array, both before and after ablation of RIG-I. Immunoblotting was performed to evaluate the levels of key molecules downstream to RIG-I leading to production of proinflammatory mediators. Changes in the intracellular viral antigen expression were confirmed by intracellular staining and immunoblotting. JEV infection induced neuronal expression of IL-6, IL-12p70, MCP-1, IP-10 and TNF-α in a time-dependent manner, which showed significant reduction upon RIG-I ablation. Molecules downstream to RIG-I showed significant changes upon JEV-infection, that were modulated following RIG-I ablation. Ablation of RIG-I in neurons also increased their susceptibility to JEV.Conclusions/Significance
In this study we propose that neurons are one of the potential sources of proinflammatory cyto/chemokines in JEV-infected brain that are produced via RIG-I dependent pathways. Ablation of RIG-I in neurons leads to increased viral load and reduced release of the cyto/chemokines. 相似文献997.
Background
Studies have suggested that CMV infection may influence cardiovascular disease (CVD) risk and mortality. However, there have been no large-scale examinations of these relationships among demographically diverse populations. The inflammatory marker C-reactive protein (CRP) is also linked with CVD outcomes and mortality and may play an important role in the pathway between CMV and mortality. We utilized a U.S. nationally representative study to examine whether CMV infection is associated with all-cause and CVD-related mortality. We also assessed whether CRP level mediated or modified these relationships.Methodology/Principal Findings
Data come from subjects ≥25 years of age who were tested for CMV and CRP level and were eligible for mortality follow-up on December 31st, 2006 (N = 14153) in the National Health and Nutrition Examination Survey (NHANES) III (1988–1994). Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for all-cause and CVD-related mortality by CMV serostatus. After adjusting for multiple confounders, CMV seropositivity remained statistically significantly associated with all-cause mortality (HR 1.19, 95% CI: 1.01, 1.41). The association between CMV and CVD-related mortality did not achieve statistical significance after confounder adjustment. CRP did not mediate these associations. However, CMV seropositive individuals with high CRP levels showed a 30.1% higher risk for all-cause mortality and 29.5% higher risk for CVD-related mortality compared to CMV seropositive individuals with low CRP levels.Conclusions/Significance
CMV was associated with a significant increased risk for all-cause mortality and CMV seropositive subjects who also had high CRP levels were at substantially higher risk for both for all-cause and CVD-related mortality than subjects with low CRP levels. Future work should target the mechanisms by which CMV infection and low-level inflammation interact to yield significant impact on mortality. 相似文献998.
Saurav Dutta Devapriya Chattopadhyay Debarati Chattopadhyay Sambuddha Misra Alexandra V. Turchyn 《Lethaia: An International Journal of Palaeontology and Stratigraphy》2020,53(3):382-395
The Kutch Basin is unique among the western Indian sedimentary basins because of its near-complete sequence of post-Palaeozoic rocks. Due to extensive marine influence, the Oligocene–Early Miocene formations of the basin, namely Maniyara Fort, Khari Nadi and Chhasra, contain numerous shellbeds. Although age assignments of these formations exist based on foraminiferal biostratigraphy, detailed numerical age of the lithounits are yet to be established. We have identified a total of eleven distinct shellbeds (oldest SB 01 to youngest SB11) from this interval primarily containing bivalve fossils. Using 87Sr/86Sr of selected oyster and pectinid shells with pristine shell characteristics, we report the age of four shellbeds. The ages of SB 01, SB 04, SB 06 and SB 10 are 24.37, 17.31, 16.85 and 15.38 Ma, respectively. Our dates suggest a Chattian (24.37 Ma) age for SB 01 from the Bermoti Member, validating the previous biostratigraphical estimates from the Maniyara Fort Formation. The Chhasra Formation, however, shows a younger range of ages (17.31–15.38 Ma) characterized by a transition from the Burdigalian (SB 04–SB 06) to the Langhian (SB 10) stages. These dates have important implications in the study of sequence stratigraphy, Palaeobiogeography and tectonic history of the Kutch Basin. A surface with subaerial exposure is found in SB 08 (between 16.85 and 15.38 Ma) that corresponds to a global eustatic sea-level decrease (Mi2). Our new dates will also help evaluate the response of marine fauna to the closure of the Tethyan seaway around 19 Ma due to the formation of ‘Gomphotherium Landbridge’. The dated shellbeds enable us to identify pre- and post-closure fauna and assess the effect of biogeographical separation on these fauna. These dates have important implications in evaluating the regional geological record of western India in the context of various global events. 相似文献
999.
Garcia-Lozano Marleny Dutta Sudip Kumar Natarajan Purushothaman Tomason Yan R. Lopez Carlos Katam Ramesh Levi Amnon Nimmakayala Padma Reddy Umesh K. 《Plant molecular biology》2020,102(1-2):213-223
1000.
Sandeep Sharma Trishna Dutta Jesús E. Maldonado Thomas C. Wood Hemendra Singh Panwar John Seidensticker 《Ecology and evolution》2013,3(1):48-60
We investigated the spatial genetic structure of the tiger meta‐population in the Satpura–Maikal landscape of central India using population‐ and individual‐based genetic clustering methods on multilocus genotypic data from 273 individuals. The Satpura–Maikal landscape is classified as a global‐priority Tiger Conservation Landscape (TCL) due to its potential for providing sufficient habitat that will allow the long‐term persistence of tigers. We found that the tiger meta‐population in the Satpura–Maikal landscape has high genetic variation and very low genetic subdivision. Individual‐based Bayesian clustering algorithms reveal two highly admixed genetic populations. We attribute this to forest connectivity and high gene flow in this landscape. However, deforestation, road widening, and mining may sever this connectivity, impede gene exchange, and further exacerbate the genetic division of tigers in central India. 相似文献